Psychobiology

Psychobiology

The biological basis of consciousness- how we perceive, act, learn and remember.

Philosophical Theories

Mentalism: Aristotle, non-material psyche. Heart= mental capacity

Dualism: Descartes 1600s, body= physical world. Mind= non-physical world, soul in the head.

Determinism, Descartes was the first physiological model of behaviour.

Physical Realm- the body is a machine- no free will- automatic reflexes.

Mental realm- mind receives info from senses- relays it to the brain-mind controls rational behaviour.

Descartes says Nerves carry spirit animals (fine streams of air that inflates the muscles). The Pineal Gland directs the flow of these spirit animals. The pineal gland is the location for the mind/body interaction.

Galvani, 1700s, Tested electrical current theory on frogs. Found that electrical stimulation made the frog's nerves move, even without a head, no animal spirits were involved. Info in the nervous system is carried via electrical stimulation.

Monism- reality is a unified whole.

Mind= biological working of the central nervous system.

Understand body >> understand mind.

Physiological or psychological thinking. Can the mind be the product of the physical brain? Evidence

Self-awareness- psychological changes in self-awareness- O. Sacks'– Asomatognosia/Visuospatial Neglect.

Mind is altered by drugs acting on the brain.

The Brain- early anatomists. The brain is composed of discrete regions. Are the regions specialised for specific functions?

Early theories

Gall (early 1800s) anatomical phrenology (measurement of the cranium to measure a persons traits). 35 domains, eg generosity, love etc. domains grew> bumps on the skull grew>> correlated with personality.

Experimental ablation (removal of body part)-

Showed specific regions for functions. Pierre Flourens (1800’s)- removed (damaged) parts of the brain to observe behaviour. simple functioning only.

Physiology of language.

Knowledge from observing verbal behaviour following brain damage.

90% of the population is left hemisphere dominant. Most language disturbance is due to damage on the left side of the brain.

Speech disorder Aphasia.

Pierre Paul Broca (1864) - Damage to the inferior left frontal lobe

Broca’s area/Broca's Aphasia

Speech output affected

laborious, non-fluent, short utterances, mispronounced

meaningful / understands

The posterior part of the hemisphere has something to say - damage to the frontal lobe = hard to express

Carl Wernicke (1876) – damage to the middle and posterior portion of the superior temporal gyrus in left hemisphere.

Wernicke’s area/Wernicke’s Aphasia

Impairment in auditory comprehension

Fluent, grammatical, but meaningless

Repeat words/sentences impaired

Often unaware of deficit

Broca's area: motor memories. Sequences of muscular movements to produce words.

Wernickes Area: memories for sequences of sounds.

Lesions to Broca's area- expressive symptoms

Lesions to Wernickes areas- receptive symptoms.

These areas must be connected to co-ordinate speech and word perception.

Conduction aphasia

– damage to connecting nerves

– speak and comprehend

– problem with repeating words, inserting incorrect words/sounds

WADA-

Test to determine which cerebral hemisphere dominates language.

This test ‘puts one side of the brain to sleep’ whilst the other stays awake. Tests each side of the brain separately for speech and language ability.

Distributed Processing-

Different components of behaviour are processed in different brain areas. Distributed processes mean the areas are working together. Central to our understanding of brain functions. 2 or more regions are involved.

Studying abnormalities of the brain and its behaviour help us to understand more typical functions.

Neurons: structure and function

Nervous system

2 divisions:

Central nervous system CNS

Brain and spinal cord

Peripheral Nervous system PNS

· Outside the brain and spinal cord

· Somatic Nervous System- Voluntary

o Interacts with the external environment

o

Receives info from sensory organs and controls muscles

· Autonomic Nervous System – involuntary

o Regulates the body's internal environment

§ Muscles, cardiac muscles, glands

Divisions of the ANS

· Sympathetic- fight or flight responses

o Stimulate, organise, mobilise energy resources

o Increase arousal, blood flow, secretion of adrenalin, heart rate, make pupils dilate

o Focused on survival

· Parasympathetic- Rest and digest response

o After flight or flight response, bodily functions return to normal rates,

o Conservation of energy, increased activity in the GI track

Protecting the CNS

Meninges, the most protected part. There are 3 layers

Protect the CNS (brain and spinal cord)

Three protective membranes are:

· Dura mater – tough membrane, the hardest of layers

· Arachnoid membrane- spider like

o Gap called subarachnoid space, filled with cerebrospinal fluid (CSF)

· Pia mater - around every surface- tender, clings to matter (tends to look like a film over the surface)

Bacterial Meningitis –

When the meninges are inflamed due to the meningitis bacteria. This can cause:

· Long-term cognitive problems

o Memory (Schmidt et al., 2006)

o Comorbidity factors - explain findings? Careful about the symptoms

o Cognitive speed (Hoogman et al., 2007) especially if left untreated

· Bacterial toxins, cytotoxic (toxic to living cell) effects from inflammation

· lead to neuronal damage (Lucas et al., 2016)

Cerebrospinal fluid- protects the CNS

provides a bouncy protective layer around the brain when in subarachnoid space , gives brain the ability to move around, and trauma is less catastrophic

4 Ventricles that are filled with CSF- This is where CSF is produced, specifically in Plexuis coroid. The central canal circulates CSF through the spine and brain.

Neurons

They are a type of specialised cell. They are receptive, conductive and transmit electrochemical signals around the brain. Their function is to detect info from the environment and ensure survival.

There are roughly 100-150 billion neurons in a healthy adult.

There are hundreds of types of neuron but the basic types are:

· Sensory Neurons (also known as afferent neurons) –

o EG, eyes detect light then these neurons take this info to the brain for it to be processed

· Interneurons- within the CNS

o Carry the message across to the relevant place

· Motor Neurons

o Send the signal to the muscle/gland so it can do its job. Neuron muscular juncture.

Structure of a neuron

The Soma - Metabolic centre of neuron

· Is the cell body

· Shape varies on each type of neuron

· contains nucleus and other structures that keep the cell alive

Multipolar Neuron;

Most common type of neuron.

Usual internal structure

The internal structure of the Soma

· Cell Membrane – cell boundary

· Nucleus

o contains chromosomes (DNA)

o portions of chromosome produce mRNA

o contains nucleolus (small nucleus inside the nucleus) = produces ribosomes

§ mRNA attaches to ribosomes – which produces proteins for cell functions, these cells will also contain DNA

· chemical reactions happen in the cell

· Cytoplasm

o semi-liquid

· Mitochondria

o Extracts energy from nutrients

o Converts oxygen and nutrients to adenosine triphosphate (ATP)

· Golgi apparatus

o Range of functions

Dendrites - Branching structures (dendron - Greek for tree)

· Function

o receive ‘messages’ from other neurons transmitted across the synapse

o Receptive input zone, receptors of a neuron

· Location - of postsynaptic receptors

Axon- Long thin tubular structure - approx. 0.2 - 20mm in diameter

· Function

o carries ‘message’ (action potentials (messages) carried electrically) away from the cell body to terminal buttons

· Myelin sheath – Covers the axon

o Insulation- which helps to transport messages a lot faster. not all neurons have them

o when the myelin starts to degrade it causes MS

Terminal Buttons

· Axons divide and branch - at the end = terminal buttons/axon terminal. The end of the neuron that can connect/meet with another

· When action potential (message) reaches terminal buttons, they secrete neurotransmitters.

· Electrical within neurons, chemical between neurons

Synapse

· The junction between neurons (between the button of sending neuron and between the receiving neuron )

· Fluid-filled gap (extracellular fluid) fluid around the neurons

o synaptic cleft (~20nm wide)

o Terminal buttons/axon terminal of presynaptic neuron forms synapse with dendrites or soma of postsynaptic neuron

o release neurotransmitters from synaptic vesicles.

o Synaptic pruning- certain synapses will be used less than others so they are basically removed. Remaining ones are strengthened.

Sending & Receiving neurons

Presynaptic cell - sending information (terminal buttons/axon terminal)

Postsynaptic cell - receiving information

Types of Neurons

· Unipolar

o one axon divides into two branches

o Most common is sensory areas

· Bipolar

o one axon & one dendritic tree at opposite ends of soma

o Common In sensitive areas in the central nervous system!

· Multipolar

o one axon - more than one dendritic branch

o receive 150,000 contacts, can have thousands of dendrites

Bipolar Neuron Unipolar Neuron

Supporting Cells

· Glia - (Greek-glue)

o Most supporting of the CNS

o Buffer neurons, keep in place, control nutrients, insulate and remove carcases of dead/injured neurons

· There are several types of Glia, such as

o Microglial cells

§ ‘Clean up crew’ (Breedlove & Watson, 2013)

§ Form a spherical zone around the damaged area

§ Help to maintain synapses

o Oligodendrocyte - in CNS

§ Support and insulate axons by forming myelin sheath - CNS

§ Surrounds many axons with myelin in segments approx. 1mm long leaving a portion uncoated (1 - 2mm)

· node of Ranvier

o Schwann cells – in PNS

§ Provide myelin for one axon

· The whole cell wraps around axon and forms one segment

§ Promote regeneration (regrowth) of damaged nerve cells (PNS)

· forms cylinders along which axon can pass

o Terminal Schwann cells maintain and repair

o Astrocytes- - CNS (Hammond et al., 2015) Star-shaped

· Maintain the blood-brain barrier & isolates brain cells from blood

o Supplies brain cells with nutrients

o Maintains brain homeostasis

· Regulate ionic composition of extracellular fluid (fluid outside the cell)

· Regulate the efficiency of synapses

o i.e. moving neurotransmitters

· Some behave like neurons, receiving and giving neurotransmitters.

Myelination

Is the same idea in both the CNV & PNS

Mid pregnancy onwards (Dubois 2014) auditory, visual and language

Demyelinating Disease is only in CNS- physical and cognitive symptoms

White Matter

Are axons with white myelin sheaths

Transmits information

Gray Matter

Cell Bodies- no myelin sheaths

Processes information

Ways we see the brain

Computerised tomography (CT/CAT scan)

X ray energy

Repeated over several angels – anatomical map

Visualise stroke, tumours (not the best for tumours)

Magnetic Resonance Imaging (MRI)

Higher resolution – radio frequency

no exposure to damaging X-ray- much safer

Cross-sectional map

Mostly works with hydrogen atoms, producing signals that computers can pick up

Can detect Subtle changes

loss of myelin (i.e. MS)

Positron Emission Tomography (PET)

Brain activity

Experimental and medical

Radioactive chemical- go into part needing to be scanned

radiation detectors map destination of chemicals

Identify regions of brain that contribute to function

Best method to detect cancer

Functional Magnetic Resonance Imaging (fMRI)

Excellent speed and sharpness

High powered to detect small changes in brain metabolism

Computer generate image for brain activity

Reveal networks of brain structures for cognitive tasks

Most used in Psychology Research

Communication within neurons: The action potential

Luigi Galvani - frog’s nerve muscle stimulated with electrical charge - transmission is electrical.

Helmholtz - speed of electrical conduction along a nerve - 90ft/sec - slower than wires

Membrane Potential

Neurons have Cell Membrane

Cell membrane creates different internal and external chemical concentrations by pumping ions.

Adenosine Triphosphate (ATP)- Energy storing molecules used by neurons to fuel the pumps.

Membrane Charge

The stored charge is called the Membrane Potential. (difference of charge inside and outside of the cell)

To figure out: Place neuron in saline solution (Sodium Chloride NaCI ) like the fluid our cells are in.

Place one micro electrode inside the neuron and another in saline solution (recording electrodes) - difference in electrical charge between the inside and outside of the membrane

Electrical stimulation of an axon

The membrane inside the brain is negatively charged at -70mV

Resting membrane potential = when the neuron is inactive the charge is -70mV

Applying a small positive charge to the neuron takes away some electrical charge (-ve) and therefore releases the membrane potential. Known as depolarisation.

When sufficient +ve charge is applied the threshold of excitation is reached. This causes rapid reversal of the membrane potential. This means the inside of the membrane becomes +ve charged and the outside becomes -ve charged. This is the Action Potential (message carried by the axon from the soma to the brain).

After the potential has passed through, the membrane rapidly turns back to its resting state but as it does it becomes Hyperpolarised (more -ve charged than that of resting state).

=ve charge applied less than the size of the reverse in membrane potential.

Generation of the Action Potential

The balance of ions diffusion and electrostatic pressure

Diffusion

Movement of the molecules from regions of high concentration to regions of low concentration - sugar dissolving in water – distributing evenly

Diffusion forces them to move to where there is less

Electrostatic Pressure

Some substances dissolve into two parts with opposing electrical charge – electrolytes – ions want to move to opposite charges

Decompose into 2 types of ions - (e.g. sodium chloride, NaCl)

cations are +ve charged ions - Na⁺ (sodium)

anions are -ve charged ions - Cl^- (chloride)

Charges repel and opposites attract =electrostatic pressure (moving ions from place to place)

Membrane Potential – the fluid inside Both contain anions and cations

Intracellular – fluid inside cell

• anions – negative charge

• Cl^- and A^- (protein)

• cations – positive charge

• Na⁺ & K⁺(potassium)

Extracellular – fluid outside cell

• anions – Cl^-

• cations - Na⁺ and K⁺

• ^{more salt outside of the cell}

Unevenly distributed meaning there is more K+ (Potassium) intracellular, and more Na⁺ and Cl^- extracellular

Balance of forces across the membrane- Why are the ions located where they are?

They aren’t even because

Passive process

Active process

Membrane semi-permeable - ion channels allow passaged of ions

But why are there high extracellular concentrations of Na⁺ and Cl^- and high intracellular concentrations of K⁺?

Cl^- higher concentration outside therefore DIFFUSION pushes in but inside -ve charge (-70mV) – therefore ELECTROSTATIC PRESSURE pushes out

As there is higher K⁺ concentration inside the cell –DIFFUSION pushes it out of the cell but the outside is +ve charged therefore ELECTROSTATIC PRESSURE pushes in. The membrane is impermeable and there is a higher concentration of A^- higher concentration inside.

Sodium Active process

Na⁺ higher concentration outside - but diffusion and electrostatic pressure pushes it in

Sodium potassium pump –

Na⁺ leaves the cell through a pump made of protein molecules - sodium potassium transporters - forces it out

Then exchanges 3 Na⁺ ions inside for 2 K⁺ ions

Uses up to 40% of neurons metabolic energy – ATP

If the ions were the same concentrations, the neurons would be unable to generate the AP

AP produced through Voltage-Dependent Ion Channels (VDI) – response to change in membrane potential allowing passage of ions (Na⁺ K⁺)

The membrane potential changes from -70mV to +40mV when the sodium-potassium pump is unable to maintain the balance so the charge goes up to +40mV. If the membrane potential is reduced to the threshold of excitation it is called Depolarisation

VDI channels for Na⁺ open and D and EP push Na⁺ in (membrane permeability increased to Na⁺)

Sodium potassium pump no longer maintains balance - membrane potential changes (+40mV)

The rapid influx of Na+ (Sodium ) triggers the Voltage dependant Ion channels so K+ can open and is driven out.

As the AP reaches its peak Na+ channels close and become refractory. This cannot be opened again until the membrane is at its resting state.

The K+ channels close slowly so too much K+ leaves the cell and accumulates outside. This is called Hyperpolarised. Eventually the K+ outside the cell with diffuse and the sodium potassium pump restores balance. The Na+ is removed and K+ is retrieved.

Absolute refractory period – a second AP cannot be produced

Relative refractory period - another AP can be started by applying a higher than normal charge.

Conduction of Action Potential

All-or-nothing Law- once triggered an AP travels the whole length of an axon, it doesn’t change size no matter how large the stimulus is as long as the threshold is reached.

However if every AP is the same size then how does the neuron signal events of different intensity?

Rate Law- there is an increased rate of firing to a stronger stimulus meaning more AP per second.

If a stimulation that is below the threshold (not an AP) we can record a small signal along the axon but no ion channels have been opened. This is Passive. Unlike a AP, the signal gets smaller, this is called Decremental Conduction and is transmitted by the cable properties of the axon.

Conduction in a myelinated axon

Mammalian axons are myelinated, this myelin sheath is tightly wrapped around the axon to prevent contact with any extracellular fluid, there is no ion exchange so the AP gets smaller. However in the gaps of the sheath, known as Nodes of Ranvier, contact with extracellular fluid is made, the small signal is enough to trigger an AP and it is regenerated, and so on between these nodes. This is called Saltatory conduction. This AP then travels under the sheath by cable properties. Myelination helps the cell to save energy and become faster.

Communication between neurons

Chemical – most neurons are connected by chemical neurons. The synapses aren’t connected chemicals work to transmit neurons.

Electrical- usually in animals

Chemical synapses; terminology (introduced by Sherrington at the beginning of 20^th century)

Presynaptic membrane - membrane of terminal button

Postsynaptic membrane - membrane of receiving neurone

Synaptic cleft/gap – tiny gap between presynaptic and postsynaptic neurons, that contains extracellular fluid

Synaptic vesicles – spherical structures in the presynaptic neuron that contain transmitters

Where are the synapses?

Most common:

Axodendritic -axon on dendrites (most cases)

Axosomatic -axon on cell bodies (Fewer cases)

Least common places for synapses to be, these are an EXCEPTION TO THE RULE:

Dendrodendritic - capable of transmission in either direction

Axoaxonic (pre-synaptic inhibition)

Chemical transmission-

Communication between neurons across synapses happens by Chemical means,

As electricity cannot just jump the gap between neurones, small chemical molecules called Neurotransmitters send the signal across. Here there has to be direct contact as chemical transmission is slower than electrical. However chemical transmission allows modifications to be made, such as the use of SSRIS, drugs, caffeine, chocolate therefore we enjoy these as they send DIRECT messages to the brain.

Types of Chemical Substances

Neurotransmitters - secreted in the synapse, only work in the synapse. 1 neuron to 1 released by terminal buttons, travels a short distance across synapse and into the receptors

Neuromodulators - (peptides small proteins) - released in larger amounts by terminal buttons to travel further. They influence many neurones and travel to receptors. Not in synapse but in outside areas

Hormones - produced and released by endocrine glands in the body, NOT the brain. For example, Epinephrine (adrenaline/ NORADRENALINE IN THE BRAIN) – travel through blood to the brain for widespread action and get to the target cells.

Oxytocin in brain is neurotransmitter, when in body it is a hormone.

Origin of the chemical substances

Small molecules (neurotransmitters) are synthesised in the terminal button and packaged in vesicles.

Large peptides ( proteins) are assembled in the cell body, packaged in vesicles, and then transported to the axon terminal

Axoplasmic transport – is an active process by which vesicles are transported from soma (Golgi apparatus) to terminal buttons along the microtubules.

Release of the transmitter substance

The AP gets created closest to soma.

When the AP is travelling along the axon it reaches terminal buttons.

Some synaptic vesicles - ‘docked’ against the presynaptic membrane, groups of specialised protein molecules in vesicle attached to protein molecules in membrane to form fusion pore. When the AP reaches the end of the axon, it brings a charge with it.

The fusion pore opens and the vesicle membrane fuses with the presynaptic membrane and releases the contents into the synaptic cleft. This process is called Exocytosis- this requires calcium. The transmitter then diffuses across the synaptic cleft towards the post synaptic membrane.

Stimulation of the transmitter release from vesicles

When the AP reaches the terminal buttons it depolarises the membrane. This is when the Voltage dependant calcium channels open.

The most important ion in cells is Calcium!

Ca²⁺ is higher in concentration outside of the cell, they flood in by diffusion and electrostatic pressure.

Ca²⁺ channels are more abundant in the pre-synaptic terminal at the level of active zones.

Ca²⁺ channels open more slowly than Na⁺ channels during the AP, so Ca²⁺ does not begin to enter the pre-synaptic terminal until the membrane has begun to repolarise. It acts as a second messenger: once it enters the terminal, the neurotransmitter is released within few hundreds msec.

The distribution of calcium is not even, there is more in the active zone as calcium is more concentrated. As it is slower to enter the cell and slower to close the cell ends up with an abundance of Calcium. This can activate various processes.

The Ca²⁺ bind with clusters of protein of fusion pores, this changes the shape of the protein, the pores are open and the membranes fuse together.

Ca activates the enzymes.

Proteins are also involved in directing vesicles to the release zones of the terminal buttons.

Pinocytosis – this process requires fine-tuned enzymes to happen.

Proteins are recycled, otherwise membrane gets larger and larger

At the junction between the axon and terminal buttons, buds of the membrane pinch off – pinocytosis

Buds of membrane fuse with cisternae, recycled to make new vesicles formed which are filled with transmitter and then migrate to release zone.

Moves because of diffusion as it isn’t charged so no electrostatic pressure. Postsynaptic potential

Postsynaptic receptors

The transmitter diffuses across the synaptic cleft and attaches to binding sites (protein molecules) these are called postsynaptic receptors.

When Receptors open channels directly, called ionotropic receptor.

When Receptor opens indirectly - metabotropic receptor - G protein and second messengers

Lock and Key Principle

The transmitter molecule needs to find a PERFECT receptor match, or it won’t work.

Ionotropic Receptors

As the postsynaptic receptors are open, the neurotransmitter-dependent ion channels are on the postsynaptic membrane, this allows ions to enter/exit postsynaptic neuron and therefore changing the membrane potential. 2 types of results of ion channels opening-

Depolarising – excitatory produces Excitatory Postsynaptic Potentials (EPSPs)

Such as Sodium (Na⁺) ion channels most importantly open, Na+ enters cell, causing depolarisation (EPSP). Calcium (Ca²⁺) produces EPSPs but also can produce structural changes.

Hyperpolarising - inhibitory – this never causes APs -Inhibitory Postsynaptic Potentials (IPSP)

The type depends on which ion channels are opened by the neurotransmitter.

Inhibitory neurotransmitters- open ion channels for:

Potassium (K⁺) - K⁺ flowing out produces hyperpolarisation

Chloride (Cl^-) - [equilibrium potential = -60] - will produce IPSPs only if membrane potential depolarised (slightly +ve) - Cl^- will enter – however at if resting potential nothing happens.

Neural Integration

An individual PSP rarely starts an AP in the post-synaptic neuron >> need for integration of signals

The interaction between the effects of excitatory and inhibitory synapses

Excitatory synapse active - produce an AP - if at the same time inhibitory synapses become active - may cancel out effects of EPSPs

The rate of firing of an axon depends on the relative activity of excitatory and inhibitory synapses

(Need to know for exam How/where did AP start- postsynaptic potential- usually multiple synapses – BOTH actives combined > called neural integration)

Termination of synaptic transmission

Neurotransmitter- Two methods:

• Reuptake - rapid removal of transmitter - from synaptic cleft - back into cytoplasm of terminal bud - active process

• Enzymatic deactivation - transmitter destroyed by enzymes - only for acetycholine - active on muscle fibres

Some meds such as SSRIs work on this.

They block the reuptake process to make serotonin linger around the synapses longer so it can be taken in.

Autoreceptors

Receptors on the terminal buttons, do not open ion channels - they are usually inhibitory when they join to the axons, stopping the inhibition process

When stimulated by the release of a neurotransmitter from its own terminal bud - it regulates internal processes to stop the release of that neurotransmitter

Self-regulation

Exceptions

Some types of communication are electrical. This kind of communication can be found in invertebrates, eg, tail flick response in fish.

Some chemical communication doesn’t happen at the synapse- receptors occur on other parts of the neurone. For hormones and neuromodulators this is the case, eg GABAA.

Electrical Communication

Physical continuity between the two cells thanks to specialised structures called gap junctions, allows direct connection between cytoplasm in the cell –and allows synchronisation of multiple cells at once.

Electrical synapses allow synchronised behaviour, for example, speed, when a squid release ink.

In humans, this type of synapse allows communication between different layers of myelin.

Kandel et al 2013 Nm= nanometers

Pharmacology of synaptic transmission and behaviour- why it is important

Many drugs act to alter neurotransmitter activity

Agonists – increase or facilitate activity

Antagonists – decrease or inhibit activity

A drug may act to alter synaptic transmission at any stage

In chemical synapses: communication is mono-directional; the released neurotransmitter binds to specific receptors on the postsynaptic membrane ("lock and key”), the binding induces changes in the membrane potential of the postsynaptic neuron.

Mate choice

o Offspring often don’t perfectly resemble parents even with asexual reproduction

o They can experience mutations that can have effects on their ability to survive

o Most of these effects will be negative- reduce likelihood of survival

o Occasionally these effects might enhance survival

o This trait is passed on to their offspring- human mutations happen very slowly

o The new form prospers

o Change happens gradually, how long depends on species reproduction rate (100 generations might be around 4 days for bacteria or viruses, but 2000 years for humans)

o Natural selection does not just affect physical features (the evolution of bodily organs)

o It also affects psychological traits (aesthetic preferences, emotional responses, problem-solving ability, food preferences etc etc)

o Peacock feathers are bad for their survival- peahens don’t have this problem. Darwin didn’t know how this helped their survival. Why was there a big difference between males and females?

o In evolutionary psychology we are often interested in ultimate questions

o What is the function of a trait in terms of its effects on survival and reproduction?

§ E.g. disgust

o Sex differences are partly the result of different mating systems

o Polygyny – common among mammals, males have access to many females (e.g. elephant seals, gorillas) males tend to be larger than females

o Polyandry – angler fish- females mate with more than one male (arachnids, bees) females larger than females

o Pair bonding -- male and females stay together to look after offspring (many birds) similar size and behaviour

o Promiscuity -- sex but no pair bonding

Sexual selection

o Competition within and between the sexes (Darwin, 1871)

o Intersexual selection: competition between males and females (e.g. males display to females and females choose)

o Peacocks, birds of paradise

o Intrasexual selection: competition between males and males or females and females

o Deer, elephant seals, stag beetles, mandrills

Female choice drives evolution- males compete - females chose model

o Selection pressure for larger and more elaborate traits

o E.g. widowbird (Anderssen, 1982; 1986) males have long tail, female doesn’t, this is because the females have chosen individual birds who have the longer tail.

o Experiment- birds in avery, 3 groups with different length tails so he could see which kind the femalw birds choose to mate with. The females tend to chose the birds with long tails as they ‘found it more attractive’ however the tail made it impossible for the male to survive. The tails signal genetic quality--

o Only healthy animals can grow large tales.

o So females are choosing for good genes (signalling theory Zahavi, 1974) as the tail is indicative of the good genes.

Why do humans discriminate in their choice of sexual partners?

Genomes are like a hand of cards

o Some cards are better than others > A good hand (good genes) is more likely to win the game of life.

o If we mated indiscriminately we might be mixing our 'good' genes with someone else's 'bad' genes, Reducing our offspring's chances of survival compared to if we (accidentally) mixed with someone with 'good' genes

o We personally do not care about someone’s genes (they’ve only been known for about 150 years)

So, if a gene/ combination of genes evolved that could determine the genetic quality of a potential partner and preferentially mate with them then that gene would increase in frequency due to greater offspring survival and this choice would evolve and become universal. We determine ones genetic qualities by physical appearance.

Symmetry (or lack of) is associated with:

o Lack of symmetry- Signs of poor parasite resistance (Little, 2001)

o Chromosome abnormalities and genetic diseases (Thornhill & Moller, 1997)

o Serious illnesses experienced (Waynforth, 1998)

o Lack of- Ill-health symptoms including concentration problems, muscle soreness, shortness of breath, backache (Shackleford & Larsen, 1997)

In essence, we find certain faces attractive because attractiveness signals good genes.

We find them disgusting because they are harmful.

Sex differences in choosiness- Females tend to be choosier than males

o Females

o High cost of sex (pregnancy, nursing, having an infant)

o Can only have a small number of children

o always certain of maternity

o Males

o Low cost of sex (can impregnate and leave)

o Can have thousands of children (potentially)

o BUT never sure of paternity whereas female are

Parental investment theory: "The sex that has the greater investment in offspring is the choosier" Rivers (1972)

Sociosexual Orientation Inventory (Simpson & Gangestad, 1991)

o There are three sections: behaviour, attitudes, and desire.

o Males are typically higher than females on all, especially the last one

o Overall the sex difference is d =.7 (big effect) This is considered large, meaning that 76% of males score higher than the average female, but notice that 24% of women score higher than the average male

Are females ALWAYS more choosy than men?

o In Jacanas (lily trotters) females are larger, more aggressive and less choosy than males- females will fight with each other for the males.

o Turns out males exclusively hatch the eggs and do more childcare

o They are the greater investing sex so the roles are reversed

What do humans look for in a mate?

o Buss (1989) sex differences are universal

o Across 37 cultures (N = 10,047)…

o Women place greater emphasis on status and wealth

o Males place emphasis on sexual fidelity and physical attraction

o BUT there are some cross-cultural differences (more equal societies have smaller differences, e.g. Scandinavia)

How big are the human sex differences?

o Sex difference in human height is d = 1.63 (Lippa, 2009)

o 'Monomorphic' (one shape- sexes are the same sizes) gibbons, sex differences in size d = .8

o So sex difference in SOI pretty the same as the difference in size in monomorphic gibbons! Not very big.

o (Stuart-Williams & Thomas, 2013

Why are humans less dimorphic (occurring in or representing two distinct forms) than their closest relatives?

o Altricial (immature) offspring caused by bipedalism and large brains- pelvis needed to be changed

o Babies are born 12 months prematurely (Martin, 1990) they have to be as they wouldn’t be able to get through the pelvis- that’s why the baby is helpless

o Therefore, two parents are required to provide for helpless babies

o This may have led to the evolution of love (for pair bonding)

o Rather than males competing and females choosing, humans may be better at adopting a strategy of a ‘mutual male choice’

Are things changing?

o More equal societies show less pronounced sex differences in mate-choice preferences (Stuart-Williams & Thomas, 2013)

o E.g. preferences for status, wealth, youth etc. Culture is clearly very important here

o Probably a lot to do with women’s education and economic independence

o Did industrialisation make thing worse?

o But will the differences ever completely disappear?

Vision

Sensory receptor: specialized neurones that alter the membrane potentials of cells when a stimulus (light) is detected. and the other types of receptors are made of specialized proteins that bind with certain molecules. This process is known as:

Sensory Transduction: sensory events are transduced (“transferred”) into changes in the cells’ membrane potential.

Transduction occurs in the photoreceptors and allows light to be converted into a change in membrane potential. This is the first part of the events that leads to visual perception, it involves a special chemical called a photopigment. This process is called:

Receptor Potential: Most sensory receptors lack axons. Instead, a portion of their somatic membrane forms synapses with the dendrites of other neurons. Receptor potentials affect the release of neurotransmitters and can modify the pattern of firing in neurons with which these cells form synapses.

Image forming: the Eye

Blind spot – no photo receptive cells but we aren’t aware of it. The brain corrects it and fills in the gaps

Cornea

The clear cornea covers the front of the eye and helps to focus incoming light. The transparent, bulbous, front surface of eyeball, protects the eye.

Light enters here and is bent inward onto the next component (the lens). This is the first stage in image formation

The Iris & Pupil

Iris: coloured part of the eye. Pupil: circular opening.

Circular muscles in the iris contract to constrict pupil. Radial muscles in the iris contract to dilate pupil. Controls amount of light entering eye. Low light – dilate, High light – contract.

Lens

After light travels through the pupil,
it must pass through the lens. The lens is responsible for focusing light on the retina. Muscles stretch the lens to accommodate different focal points in the outside world. Lens becomes less flexible with causes long-sightedness with age (presbyopia)

Short- sightedness Long- sightedness

Glasses correct and change focal length of the lens

Short sighted- focus point falls short of the retina

Long sighted- focal point is behind the retina

Retina & Fovea

Retina: thin light-sensitive lining on back of eye. Part of the central nervous system

Fovea: Centre of the
retina. Fovea has the highest density of photoreceptors and is responsible for all colour vision and all fine vision.

Optic disc causes blind spot.

The eye moves 3 times a second in order to shift it onto interesting things​ - We’re effectively blind during these saccades.

Photosensitive lining at the back of the eye- bit of the eye that is like the film is the back of the eye (optical nerves)

Fovea has the highest concentration so when you look at something directly you get the most accurate images

We perceive a seamless world but the eyes are always moving to find the interesting things to look at.

Transduction

Light-sensitive cells are at the back, unlike animals where its switched. Light processing starts in the retina.

Light comes in, hits light-sensitive cells and causes a chemical AP that then goes through the rest of the wiring via transduction and down to the rest of the brain.

Only light specific action occurs in the back of the eye> after this it is a normal cell process.

Ganglion cells same as brain ganglion cells

Visual Transduction: Rhodopsin

The pigment found in rods. Opsin is found in cones

When the light goes in the cells stops the firing. When its dark the cells fire>

When there’s an object, or ‘danger’ the AP fires because of the dark

A G protein-linked receptor that responds to light rather than to neurotransmitters

In the dark- Na+ channels remain partially open (partial depolarization), releasing glutamate

When light strikes, Na+ channels close

Rods hyperpolarize, inhibiting glutamate release

Vitamin A is a precursor of the main compound of the visual system. It cannot be synthesized. (carrots)

Photoreceptors

Dark adaptation refers to the process whereby the retina adapts to decreasing levels of illumination, which entails a transition from a cone to a rod activity, and thus a change in light sensitivity

After passing through the lens, light traverses the main part of the eye, which is filled with vitreous humour, a clear, gelatinous substance. After passing through the vitreous humour, light falls on the retina.

Neural communication post-transduction

Photoreceptors and bipolar cells do not fire action potential but release neurotransmitters in a graded fashion.

Action potentials only occur in the ganglion cells. After the light receptors have been fired

The output of the retinal circuits is about 20 ganglion-cell types

Already these carry different representations of the external world. Processing starts in the eyeball

Visual pathway through the brain

Light comes in and starts the process of transduction. The electrical signals go to back of the brain, V1

Each area the vision travels through info gets more abstract.

Light entering the eye is focussed onto the retina. Light is converted into electrical signals by photoreceptors

Retinal cells extend into the midbrain (LGN)

Information is then passed onto visual cortex

2 visual pathways/systems

One for ‘seeing’ what we look at

One for controlling where to look

Retinotopic Organisation

Visual fields are KEPT SEPARATE

Contralateral- the side of the body opposite to that on which a particular structure or condition occurs.

Ipsilateral - the same side of the body on which a particular structure or condition occurs.

M (Magnocellular) big

M cells carry motion-related information

Fast Response - Also called parasol - Input mainly from rods photoreceptor cells and therefore are sensitive to brightness

P (Parvocellular) small

P cells carry colour and fine detail

Slow response - Also called midget - Input mainly from cones photoreceptor cells mostly and therefore are sensitive to colour

Other classes include

Bistratified (Project to Koniocellular pathway)

Photosensitive ganglions (involved in wakefulness)

Two visual pathways – only one with conscious access

Goodale and Milner 80/90

Patient DF – visual form agnosia

Dorsal and Ventral pathways

The dorsal stream controls action and is not accessible to the consciousness back of the brain

Ventral stream is dedicated to perception of visual world ventral to ventral contact, front of body

Double Dissociation: Recognition & Action

Visual Form Agnosia (“What” damage)

DF (Milner & Goodale, 1995)

Cannot recognise objects by sight but can by touch- But has intact visuomotor control

Cannot match the orientation but Can “post” a card into slot

Visual Ataxia (“How” damage)

Object recognition unaffected - Can match but cannot post

Researchers had rotating letter box

DF- can tell you about it in the letter but they can't physical post it

Visual Ataxia- could post the letter but couldn’t tell you about it. We don’t know if this happens with ppl who don’t have brain damage?

Haffenden and Goodale – experiment using Ebbinghaus illusion

Verbal reporting and measurement of finger preparation when subjects attempt to pick up 3D models of the illusion

Made Ebbinghaus illusion with card- ask to pick up the card and they were able to perceive how big the inner ball was.

Ventral part started with thinking the ball was big so makes the fingers wider apart and dorsal part takes over when the fingers get closer to make the space narrower

Dorsal and Ventral Streams

Ventral stream (purple)

Projects to the inferotemporal cortex (ITC) & Ventral temporal cortex

The “What” stream & both P (perception/colour) and Motion cells

Dorsal stream (green)

Projects to Posterior parietal cortex (PPC)

The “Where” stream - mainly Motion cells

Ventral Pathway (purple, under occipital lobe)

ITC (Inferotemporal Cortex) - primary centre for object recognition – in the hippocampus & PFC (working memory, recall of visual memories & amygdala

Has an anterior and posterior part with columnar organisation. Face selective cells can be organised in specific clusters (monkeys- at least 5 different inter-connected areas, each specialised for different aspects of facial recognition)

Dorsal Pathway (green, above occipital lobe)

Allocation of visual attention – localised objects in the visual scene/computerised motor programs to interact objects (grasping objects ect). The anterior part of the stream merges with the Motor cortex and comprises neurons with both visual AND motor functions (mirror neurons). Don’t have conscious control over it, mainly comes from practise.

Brain damage Studies and functional-imaging studies suggest that these special face-recognizing circuits are found in the fusiform face area (FFA), located in the fusiform gyrus on the base of the temporal lobe

Secondary and Tertiary (third order) visual areas

Located in V2& V3 (Broadman's area 18/19 )

Motion Perception

Located in V5 - Simple neural circuits allow simple motion to be detected in retinal cells

(Bilateral damage to the human brain that includes area V5 produces an inability to perceive movement, can happen with damage to occipital cortex and V5 area—akinetopsia)

Rods are particularly well suited But Aperture problem (full understanding of motion requires integration of many local signals)

Self-motion - need to subtract visual motion caused by own movements

Neuropsychology of Vision

Unilateral visual neglect

Usually happens due to brain damage – ppl can only see ONE side of their view

Participants asked to describe town square (Piazza del Duomo in Milan) from the North, then to do it again from the South – each time only half of the view (Bisiach and Luzzatti 1978) Bisiach and Luzzatti (1978) asked patients with left-sided visual neglect from Milan to imagine viewing the central square, the Piazza del Duomo, from the cathedral in the centre of the square. Could only imagine stuff from the right hand side of their perception

Not eyes that are the problem it was their covert attention. Not aware they had that impairment

Posner argues that an impairment of covert visual attention

Blindsight:

90% of optic nerve fibres project to the Lateral Geniculate Nucleus of the thalamus then to primary visual cortex (V1, striate cortex, Brodmann area 17)

10% of optic nerve fibres project to pulvinar of thalamus then on to superior colliculus (control of eye movements)

Eyes work fine but its brain damaged. Put them in front of light and guess where light it. The conscious part is damaged but the unconscious part isn’t damaged so they were fairly accurate. Geniculo-striate pathway. Colliculo-parietal pathway

Prosopagnosia - failure to recognize people known to the patient on the basis of visual perception of their faces" (Grusser & Landis, 1991) Prosopagnosia inability to perceive global whole of face – attention.

(Bodner, 1947) coined term

Other modalities intact – can recognize voices

"The Man Who Mistook His Wife for a Hat". Although Mr. P could not recognize his wife from her face, he was able to recognize her by her voice.

may actually reflect a more general inability to recognize individual feature or members of a more general category. Examples of this include a person who is unable to distinguish their car from others, or a bird watcher who can no longer recognize different species of birds may recognize a facial expression. Couldn’t recognise human features - don’t see faces at all. May use distinctive facial features to compensate; Mr P (e.g., his brother’s chipped tooth). Therefore can see the detail

Typically associated with lesions in the right IT cortex

e.g., Fusifor gyrus: Evolved for face recognition (Farah et al., 1995). Inversion effects

inferior-medial temporo-occipital area of the brain. Can see where the damage is in MRI

Implicit Face Recognition in Prosopagnosia

Familiarity of unrecognized faces can influence skin conductance (Bauer, 1984)

Cannot identify pictures of family & famous faces BUT electrodermal responses greater than chance. TILL have an emotional reaction to ppl they do know, dorsal part of the brain gives the emotional reaction of seeing ppl they know.

Capgras Delusion: Symptoms

Man had brain damage- wife came back and recognized her but didn’t have the emotional (dorsal) reaction so diminished responsibility and he killed her.

Prosopagnosia & Capgras Delusion

Ramachandran & Blakeslee (1997)

Damage to the visual pathway

V1: Scotoma in contralateral visual field.

Blindsight - Visually guided behaviour but no visual awareness

Ventral pathway - Agnosias (e.g., prosopagnosia)

Dorsal pathway - Akinetopsia (motion blindness) at V5. Unilateral neglect. Optic ataxia

Bottom-Up Processing

Cog process- simple processes that build up to complex higher processes. (outside in).

J.J. Gibson (1966; 1979) argued that what we perceive is directly determined by the information in the visual scene and that no higher-level cognitive processing is necessary.

Direct perception through properties of the optic array can build up everything we know about the world. This is all the light that falls on our eyes from every direction. Evolutionary angle explanation for how optic array carries information

Object Recognition in Nature

Simple mechanisms of recognition - Tinbergen (1951) - sticklebacks ignore very realistic models that don’t have red underbellies, and recognise very unrealistic models that do have red underbellies – they will ONLY recognise another stickleback when it DOESN’T look like them but humans do the opposite - why?

Receptive Fields

Receptive field of a visual neuron is the area of the visual field within which it is possible for a visual stimulus to influence the firing of that neuron

You can measure a receptive field for all the different levels: Retina, LGN, Visual cortex and so on... Every cell has one

Visual system neurons tend to be continually active; thus, effective stimuli are those that either increase or decrease the rate of firing.

Hubel and Wiesel won the Nobel Prize (Physiology or Medicine 1981) for mapping these kind of responses in cells in feline visual cortex

Ganglion Cells

In the 1930's Hartline discovered that the retina contains 3 types of ganglion cells:

On cells: these respond when a light strikes the retina

Off cells: these respond when the light is removed

On/off cells: these respond briefly when the light is on and also again briefly when the light is switched off

Stimulation of the centre or the surround had different effects depending upon the type of the cell. In the 1950's Kuffler recorded the activity of retinal ganglion cells and discovered that their receptive fields are in the form of a central region surrounded by a concentric circle.

One/Off centre Cells

Receptive fields overlap which ensures that a small spot of light will excite or inhibit many ganglion cells - this is how we determine shapes.

Bar and Edge Detection

Relies on animal experiments- cat was unconscious- eyes kept open > Looking at rotating bars>

neurons in the visual cortex selectively respond to specific features like contours of the visual world, indicating their involvement in bar and edge detection.

Building up shapes from simple calls:

Hubel and Wiesel (1962) – low level feature detectors

On- light hits the middle, firing rate goes faster

Off- firing rate goes slower

Building shapes from simple cells, bar detector complex cells

A bunch of ON cells aligned together > detects bars.

Building shapes from simple cells edge detector complex cells

Only get to see an edge if all ten cells fire which then fires the next cells

Simple Cells

Simple cells respond best to a line of: specific size cells, cells in a specific orientation and cells in a specific place. There is high firing when the bar is in the RIGHT place

Simple Cortical Cell example

Three adjacent LGN
neurons feed cortical cell

When all three centres are stimulated cortical cell
fires like crazy. Same line in different orientation – not interested

Simple Cells

Different arrangements of receptive field allow different orientations to be encoded by simple cells. Enough simple cells, with increasingly complicated inputs
can encode almost anything

Edge detection- on their own would be enough to navigate. Often the most important part of an image. Millions of the cells in the brain are specifically for bar and edge detection, there are cells for every possible direction - trained from birth.

Hypercolumns

Complex cells - Similar to simple cells

More common than simple (75% of V1)

Respond best to a particular orientation But They have a larger receptive field and arent so fussy as to location. Some are direction selective – respond best to movement in a particular direction across their receptive field. Many are binocular – respond to input from either eye

Modular organisation of V1- Organised into 6 layers

Cells in different layers receive signals from different LGN layers - Different layers project to different (extra-striate) destinations

Orientation preference is organised by column

Ocular dominance – Left vs Right eye alternates horizontally - Blobs analyse colour

Pandemonium: an Artificial Intelligence application that possesses a hierarchy of increasingly complex features

Lower-level demons fire when hyper columns are fired (In cheques- the numbers are written in a way that computers are able to recognise)

Hyper-columns CANNOT explain how complex objects are Perceived by natural organisms (such as humans)

NO, simple features are NOT built up into ever more complex and abstract features. This is not how it is believed that object recognition occurs in humans. Single neurons don’t represent abstract objects (like your Grandmother or yellow volkswagens). Bottoms up meets top down to recognise simple features of the car.

Single neurons don’t code for every single thing we see-

Hyper columns have cells beneath then that feed into other cells receptive fields. >

There are limits to it, where bottom-up processing doesn’t work anymore

Top Down Processes

Existing Knowledge (from inside to outside)

Top-down processing is a way of explaining a cognitive process in which higher-level processes, such as prior knowledge, influence the processing of lower-level input.

Memories or knowledge will influence what, and how, we perceive.

Takes perception to be:

Not just sensation, but an active and constructive process.

A direct by-product of sensations and hypotheses about the world and how it works.

Influenced by individual differences and personal experiences.

Visual illusions –

Work from visual expectations for the world . Top-down process giving incorrect information.

If you stare at one spot then the image there is not moving. It appears to move because of the difference in luminance between the bits that are next to each other (e.g. if you squint, you will see black and which and they are not moving).

The Hermann

The Hermann grid illusion is an optical illusion reported by Ludimar Hermann in 1870. The illusion is characterized by "ghostlike" grey blobs perceived at the intersections of a white (or light-colored) grid on a black background. The grey blobs disappear when looking directly at an intersection.

The effect of both optical illusions is often explained by a neural process called lateral inhibition. The intensity at a point in the visual system is not simply the result of a single receptor, but the result of a group of receptors which respond to the presentation of stimuli in what is called a receptive field.

A retinal ganglion cell pools the inputs of several photoreceptors over an area of retina, the area in physical space to which the photoreceptors respond is the ganglion cell's "receptive field". In the center of the receptive field the individual photoreceptors excite the ganglion cell when they detect increased luminance. The photoreceptors in the surrounding area inhibit the ganglion cell. Thus, since a point at an intersection is surrounded by more intensity than a point at the middle of a line, the intersection appears darker due to increased inhibition. - There is strong evidence that the retinal ganglion cell theory is untenable. For example, making the lines of the grid wavy rather than straight eliminates both the Hermann grid and scintillating grid illusions. The Baumgartner / RGC theory does not predict this outcome. Lateral inhibition theory also can not account for the fact that the Hermann grid illusion is perceived over a range of bar widths. Lateral inhibition theory would predict that decreasing the size of the grid (and therefore decreasing the amount of inhibition at the intersection) would eradicate the illusory effect. One alternative explanation is that the illusion is due to S1 type simple cells in the visual cortex.

The Scintillating Grid

The scintillating grid illusion is an optical illusion, discovered by E. Lingelbach in 1994, that is usually considered a variation of the Hermann grid illusion.

It is constructed by superimposing white discs on the intersections of orthogonal gray bars on a black background. Dark dots seem to appear and disappear rapidly at random intersections, hence the label "scintillating". When a person keeps his or her eyes directly on a single intersection, the dark dot does not appear. The dark dots disappear if one is too close to or too far from the image.

Top-down processing in colour perception

What colour we perceive is not a straightforward reporting of the wavelength of light coming into our eyes

Perceptual constancies are sources of illusions. Colour constancy and brightness constancy are responsible for the fact that a familiar object will appear the same colour regardless of the amount of light or colour of light reflecting from it. An illusion of colour or contrast difference can be created when the luminosity or colour of the area surrounding an unfamiliar object is changed. The contrast of the object will appear darker against a black field that reflects less light compared to a white field even though the object itself did not change in colour. Similarly, the eye will compensate for colour contrast depending on the colour cast of the surrounding area.

Biasing effect of existing knowledge

Bottom-up – by looking at its parts

But maybe there is ambiguity

Top down – also considering context

What is context?

is other letters surrounding each letter

is other words surrounding each word

is overall meaning of passage (including expectations about comedy, irony etc)

Considering all these aspects of context involve checking contents of long term memory

Bu processing tells us theres 2 A on the image

Top down context tells us that there is only one. We disambiguate the letters

Why is bottom-up not good enough on its own?

The bare sensory signal we get in vision is consistent with a large (infinite) number of arrangements of the real world

So it we want to know what real world situation did actually give rise to our sensory signal we have to make inferences

We can disambiguate by:

Getting more information from the world

E.g. moving ourselves to get motion cues

Deploying stored knowledge about the world

Using top-down information from memory

We perceive the world in our own context

Bottom up and top down working together

The brain combines prior expectations with incoming sensory evidence to produce a percept that is the best available hypothesis on the state of the world

But what is balance between bottom up and top down?

Predictive processing claims that conscious perception is more strongly tied to top down processes

we perceive the ‘expectation’ that is a simulation created by the brain, and that simulation is modulated by the sensory input

"Small Modulations of Ongoing Cortical Dynamics by Sensory Input During Natural Vision", József Fiser, Chiayu Chiu and Michael Weliky, Nature. 2004 Sep 30; 431:573-578)

These results suggest that in both the developing andmature visual cortex, sensory evoked neural activity representsthe modulation and triggering of ongoing circuit dynamics byinput signals, rather than directly reflecting the structure of theinput signal itself.

Predictive processing – differences with traditional view

Traditional view

Perception as just bottom up feature detection

Visual cortex is hierarchy of neural feature detectors with neural population responses driven by bottom up features

Step-wise build up from simple to complex in lego-block fashion

Brain = passive and stimulus driven – Sat watching things appear in front of you

Hierarchical predictive coding

Percepts emerge via a recurrent cascade of top down predictions spanning multiple spatial/temporal scales

Downward predictions reflect expectations on inputs what your seeing is what your brain predicts you should see. When its wrong the system gets updated

Unsupervised learning of the world – bootstrap heaven

Model out whats going to happen,

Delusions - idea that ppl with schizophrenia- Top down processing that recognizes faces

Predictive processing-

Predictive processing avoids the need to process huge amounts of information in a serial, incremental fashion

Using stored knowledge to predict the current sensory input

Only processing deviations from the expected multi-level flow

Algorithms actually first developed for data compression

But not so hierarchical in this application

cf Minsky’s 1960s claim that all computer vision could be achieved in one summer by an MSc student

We perceive a model that is created from our previous experience

Delicate process

Would not do to always see what we expect

Sensory signals and existing model are weighted

internal representations provide a constant stream of predictions about what the perceptual system should actually being perceiving from the basic sensory data the organism receives.

All the time there is a mismatch between model derived prediction and actual perception the model is updated to minimise the error.

What happens when weighting goes wrong?

‘Perception is co-emergent with imagination’

‘Perception is controlled hallucination’ – if we rely too much on it it can cause hallucination

Reward Mechanisms

How does stimuli control behaviour?

Classical Conditioning :

US; when were hungry we get hunger pains, we eact the food and then feel rewarded, high fat sugery foods give more of a response

CS- eventually becomes a conditioned response

Quicker the response/ reward the quicker it is learnt

Operant Conditioning:

Not all behaviours are Unconditioned Responses

l some are actions on the environment

l behaviors change with experience

Ø Instrumental learning:

l learning the connection between a behaviour and consequences

Law of effect: Several responses made in a situation

pleasant outcome = increase in occurrence more pleased you get,more likely you will be to repeat the behaviour - unpleasant outcome = decrease in occurrence

Reinforcment

Ø Natural reinforcers

l food, sex

Ø Abnormal reinforcers

l compulsive behaviour pharmacological

Ø Positive (rewarding with praise, bonuses etc)

Ø Negative (remove adverse experience, eg painkillers for headache, putting suncream on to avoid getting burnt)

l money, praise

Ø Punishment – positive(giving) /negative (removing)

l Positive - fines, negative- removing privileges

Brain mechanisms responsible for reinforcement

Olds & Milner (1954)

l Animals work for electrical stimulation

• Intracranial self-stimulation (ICSS) animals will press a lever for the stimulation of these rewards

• Ignore natural reinforcers – food, water

PATHWAYS

l Direct transcortical mid-brain areas

l and via basal ganglia and thalamus

Brain Regions:

Highest rate from septal area, amygdala (emotions) & anterior hypothalamus

(in terms of the rats, they get the rewards more in the places of the electrodes Moderate rates from limbic structures hippocampus, cingulate gyrus, anterior thalamus, posterior hypothalamus, Primitive behaviour, guides and motivates behaviour

Medial Forebrain Bundle (MFB)

Stimulation of MFB - intense pleasure - more than any other region

Intracranial self-stimulation (ICSS)

Ø Connections between ventral tegmental area (VTA) and lateral - hypothalamus processes

The reward circuit lies within the MFB

l is a substructure consisting of:

• mesolimbic pathway - VTA -nucleus accumbens

• mesocortical pathway - VTA - prefrontal cortex

• connections to amygdala & septum (septal area)

Role of Dopamine in Reward

Ø MFB stimulates dopaminergic systems pathways, receptors within the brain

(Phillips & Fibinger, 1989; Wise et al., 1987)

Three subdivisions

Ø Nigrostriatal pathway- important for movement, rich in dopamine- present in parkingsons

Ø Mesolimbic pathway – MFB

Ø Information from VTA, amygdala, hippocampus to nucleus accumbens (forebrain reward centre) mcb runs through

Ø Mesocortical pathway–

Ø VTA to frontal and limbic cortex and hippocampus-

MesoLimbic Pathway

Ø Two mid-brain nuclei

l substantia nigra (SN) – includes NA

l ventral tegmental area (VTA)

Ø Rich in dopamine -- projected to forebrain sites

Ø Not reliably activated by pleasure due to Individual Differences but also got to want the reward from the stimulation,

The primary role of the Mesolimbic pathway (Robbins & Everett 2007)

l incentive salience how important it is for you

l arousal

l Motivation/ anticipate the reward

l memory consolidation, have to make the connection between what happened and when

Evidence for the Dopamine Pathway

Ø Electrical stimulation of SN & VTA, MFB or VTA

l rewarding - areas high dopamine neurons (Corbett & Wise 1980)

l release dopamine in NA

Ø Reinforcing events activate NA

l Social reward, reinforcing events /avoidance punishments (Kohls et al., 2013)

l Gains in reputation and Facebook use (Meshi et al., 2013)

Ø Dopamine Antagonists drugs that block dopamine, no reuptake

l block dopamine receptors in NA

l interfere with reinforcement - reduces ICSS (Stellear, et al.,1983)

Ø Dopamine agonists facilitate the actions of dopamine

l enhance reinforcement

l self-administer 'addictive'

l Conditioned Place Preference – dose of amphetamine

Conditioned place preference- place rat in box with multiple areas, if they receive a reward in a specific box, they tend to stay in that area and naturally gravitate towards it

Functions of reinforcement system

Ø Reinforcement system - 2 functions

l detect potential reinforcing stimulus

l strengthen connection

l between neurons that detect the particular reward stimulus and the response- really important to motivate the particular behaviour

Detecting reinforcing stimuli

Ø Neural circuits detect reinforcing stimuli - activate Dopamine neurons

Ø Dependent on motivational state (and individual differences)

l hungry animal will detect food

l satiated animal will not

Ø Reinforcement system activated by unexpected reinforcing stimuli

Dopamine and neural plasticity - Instrumental conditioning = 3 elements

1. Discriminative stimulus

2. Response

3. Reinforcing stimulus

Dopamine therefore facilitates synaptic strengthening (Stein & Belluzi 1989)

Location of Synaptic change-

Input to VTA from the amygdala, lateral hypothalamus, and prefrontal cortex. NA neurons send axons to regions involved in movement > basal ganglia(lesions can disrupt learning), prefrontal cortex > Lesions to basal ganglia disrupt instrumental learned behaviours

Ø Medial Prefrontal Cortex (mPFC)

l responds to the outcome of reward what actually happening, encodes response

Ø Orbitofrontal cortex (OFC)

l encodes expected outcomes helps judge the potential emotional value

l estimates emotional value of potential reward

Ø Ventral striatum (VS)

l saliency, valence, predictability- how likely is it to be rewarding

Helps to evaluate rewards from the behaviours we do, Important in rational decision making, sometimes we have to inhibit certain behaviours. Goal-directed behaviours

Developmental Aspects of Reward

Ø Pruning & changes in functional connectivity

l Children – VS activity but less frontal to reward stimuli more governed by rewards and not rational and goal directed behaviours – less brain maturity but more plasticity

l Adolescence – VS and mPFC activate (Bjork et al, 2004) start to organise and control behaviour

Risk Taking

Heightened risk taking - why?

l Enhanced sensation seeking? May want to take more risks

l Less aversive biological responses?

Ø Adolescent rats–less motor impairment/ hangover!

l Hypo & hyper-responsive striatal system

l Evidence tends to lead to hyper response, overly responsive to the rewards, gaining more pleaser

Ø Increased dopamine activity

l PFC - Rewarding stimuli - more rewarding? Taking risks is felt as more rewarding

Ø Risky behaviour decreases

l Maturation of cognitive control system? (Steinberg, 2008) the older u get, you get more better at controlling behaviour and rational thoughts

l More car accidents similar aged passengers (reverse for adults) adolecenes close to age when they pass are more likely to have crashes

Peers – Chein et al., (2011), fMRI, simulated driving

l adolescents (13-16), young adults (17-24), adults (25+)

• Alone - adolescents similar number of risks as adults

• Peer observation –adolescents risks tripled; young adults doubled

Ø Adolescents

l > activation reward regions (VS, OFC)

l Level of activation predicts risk-taking the more activation correlated with an increase in risk taking

Ø Adults

l no difference in VS/OFC between peer and non peer observation

l > recruitment areas (LPFC) - cognitive control

l Able to evaluate the consequence and inhibit the resppnse if risk is to great

Music and Reward

Ø Music activates the dopaminergic mesolimbic system (Sihvonen et al., (2017)

l NA – regulates mood and pleasure

Ø Neurotypical

l mesolimbic activation from intense emotional response to music = increased release of dopamine (Salimpoor et al., 2011)

Ø Neurological disorders

l Music therapy benefits – e.g. Stroke, Dementia, MS,

Ø dopamine = improved cognitive-emotional gains - music therapy

l improved mood = enhanced cognition in neurological patients

When in a positive mood, more likely to perform better in cognitive tasks. An increase in dopamine- there may be an increase in dopamine and helps cognition

Drug Use and Addiction

Medial Forebrain Bundle (MFB)

Ø Lateral hypothalamus

l powerful area for intracranial self stimulation-

Ø MFB

l diffuse system of fibres

l connects limbic system to other regions of brain

Ø Incorporates midbrain dopamine (DA) pathway inc. mesolimbic DA pathway

Pre Frontal Cortex - judges whether the reward is worth it or not and evaluating whether it will be successful

Mesolimbic dopamine pathway

Ø Two midbrain nuclei

l substantia nigra & VTA

Ø Rich in DA & project to forebrain inc.

l Lateral hypothalamus, preoptic area, NA

Ø Stimulating MFB

l Activates DA reward circuit

Ø DA antagonists in NA reduces effect of MFB stimulation (Stellar, et al., 1983)

Stimulating MFB (spec nta) stimulates the rewards circuit- stimulates dopamine release

Ø Dopamine antagonists- block the dopamine receptors- can reduce the reward of MCB and inhibit feelings o frewards

Reward Systems

Ø Rats commonly used for research (similar brain chemistry to us)

Ø ICSS in certain areas of the brain (Olds & Milner, 1954)

l Rats will press a lever as rapidly as 2000 times each hour

l Ignore natural rewards

l Any stimulation in area will make them ignore natural stimulation

Addiction

DSM/ICD

Ø Key criteria - at least 2 - 3 of....

l difficulties in controlling substance use interlinked with the craving

l craving

l Tolerance has to be this for diagnosis

l effects of acute withdrawal desensitised brain

l neglect other interests, social and family activities despite knowing the negatives

l continued use despite knowledge of physiological/psychological harm

Rogers (2017) - A substance should not be labelled as addictive or non-addictive

l does not affect everyone

l coffee - low risk - nevertheless, 'caffeine addiction'

l rewarding foods - energy dense

Ø carrot addiction! Generally foods with more sugar, comfort foods

Ø behavioural pattern of drug use, characterised by overwhelming involvement with the use of a drug (compulsive use), the securing of it’s supply and a high tendency to relapse after withdrawal.

Ø Addiction is viewed as an extreme on a continuum of involvement with drug use and refers to the quantitative rather than the qualitative sense to which drug use pervades the total life activity of the user and to the range of circumstances in which drug use controls their behaviour.

Addictive Drugs

Ø Affect DA neurons in MFB

l opiates

l cocaine & amphetamine

l nicotine

l alcohol

Ø Research in non-humans - Drug self-administered paradigm rat places in box, able to self-administer drugs

• Conditioned place preference learn to spend time in the box where they get the drugs

• excites reinforcement system

Drug Dependence

Physical dependence

l adaptive state

l Increased experience = reduced drug action > tolerance

l Cessation of drug-taking = intense physiological disturbance > withdrawal

l typically, opposite of drug action

Brain starting to rewire – to become addicted there MUST be some sort of dependence

Repeated use will cause the brain to desensitise which leads to detolerance so need more to get a high

If they suddenly stop they will go through withdrawal- often opposite effects of the drugs- withdrawal is so strong that can cause gastrointestinal prombles

Psychological dependence

• Condition

• Pleasurable state

• Motivated to take drug to maintain a pleasurable state or avoid discomfort

• negative reinforcement

Gained from positive feelings that the drug induces- negative reinforcement (removing unpleasant consequences) motivated to continue taking as they will have the bad effects

Withdrawal Varys in relation to substance

Intense physical disturbances

Appear when habitual administration is interrupted

relatively independent of individual & environment

Escape & avoidance of withdrawal effects - role in maintaining drug use despite knowing the bad side effects etc

Compensatory mechanism

Tolerance

Decreased sensitivity

Desensitisation = tolerance

Two components

• Continued use - less effect

• Tolerance develops - increasing doses must be taken

• psychological and physiological effect

Homeostatic mechanisms – doesn’t like to be out of balances- eg too cold, too hot- drop/ rise in blood sugar-

Over time the brain will desensitise itself as it cant cope with the inbalance inside the body – it will damped down the effects so it doesn’t feel the inbalance –

When it is desensitised it becomes tolerant to the drug > Motivates the person to have more

Ø Downregulation

l the desensitisation of receptors OR

l decreased dendritic branching

• NA (Russo et al., 2010)

Ø In pavlovian conditioning behavioural tolerance, the brain expects it to happen

l instrumental behaviour and non-associative mechanisms (habituation) = behavioural tolerance

Over continued use of substance causes the sight of the stimulus to cause the brain to start the compensatory reactions as it knows that it may be coming

Overdose- if the stimus has changed and the person has taken a large dose, the brain isn’t ready and hasn’t got the compensatory response

Neural Changes

Drug-induced neural changes - Rogers (2017)

l cortical and basal ganglia

l DA pathway

Ø Critical for dev. of addiction

l neural changes characterise transition from =

• occasional/voluntary drug use → habitual use → compulsion → chronic addiction

Opiates

Ø Chemicals derived from opium poppy

Ø Opioid refers to opiate like substances

Ø Dried opium powder contains more than 20 alkaloids of varying psychopharmacological potency

Ø Principle active compound is morphine

Ø Second active compound is codeine

Heroin

Ø An opiate alkaloid derived from morphine

l strongest of the substances

Ø Opium poppy opioids mildly addictive in the form of morphine

Ø Heroin intravenously

l extremely addictive

l intense physiological & psychological reaction bc the reaction fron the IV heroin use occurs almost immediately after administration

Effects of Opiates

Ø Emotional changes in mood, functions of CNS and bowel

Ø Analgesia, drowsiness, mood changes, mental clouding, reduced movement and secretion of the GI system (nausea, vomiting)

…On Brain Reward Systems

Ø Opiates stimulate opiate receptors

l DA neurons of reward system

Ø Opiate receptors present in VTA and NA

Ø Opiates release DA in NA (MFB)

l reinforcing effects of opiates

Ø Animals press lever for IV opiate

l either ends of mesolimibic pathway VTA and NA

Ø However: Opiates reinforce via activation of NA alone, itll do bothbut opiates seem to function closer to NA

Ø Learning & reinforcement

l produced by activating neurons in mesolimbic system and releasing DA in NA

Cocaine and Amphetamine

Ø CNS stimulants

Ø produce a mild elevation of mood, increased energy, alertness, mild suppression of appetite

Ø Amphetamine was first synthesized in the 1920’s

Effects on Brain Reward System

Ø Cocaine & amphetamines stimulate mesolimbic DA pathway - agonist

l Cocaine inhibits DA transporter

• increases extracellular DA

l Increases effectiveness DA synapses

Ø Amphetamine

l blocks reuptake and increases release of DA

Ø DA synapses

l responsible for euphoric/addictive properties (Wise & Bozarth 1987)

Ø Single dose of Amph. in addicted rats increases DA in NA (Sato 1986)

Ø DA antagonists & destruction of DA terminals of NA

l stop effects of cocaine & amphetamine

Purified Cocaine & Amphetamine

Ø Coke, freebase (crack)

Ø Low doses

l effect depends on envi. & psychological makeup

Ø Higher doses

l effects of envi.& individual experience less important

Dosage level matters in how ppl cope and what they experience

Effects

Ø Euphoria, enhanced physical & mental capacity, reduced need for sleep/food

Ø Tolerance

Ø Toxic symptoms

Ø Paranoia

Ø Perceptual abnormalities

l skin sensations

Nicotine

Ø Stimulates VTA DA neurons of mesolimbic pathway

Ø and release DA in NA

Ø Binding to nicotinic acetylcholine receptors located on DA neurons

Ø Nicotinic agonist into VTA reinforce conditioned place preference

Ø Although nicotinic receptors in VTA & NA, nicotinic agonist in NA = no reinforcement

Ø Nicotinic antagonist into VTA reduce reinforcing effects

Ø but not in NA

Taken together - opiates, cocaine and amphetamines are addictive > produce profound emotionally compelling sensations > modify activity of DA brain reward system – mesolimbic DA system

Recent Developments

Ø Addiction is Psychologically complex

Ø Addiction involves many parts of the brain

l Prefrontal cortex

• Poor decision making, risk taking

Ø Addiction involves many neurotransmitters

l eg Glutamate, norepinephrine, serotonin endogenous opioids

Ø Addiction is not limited to drugs

l Compulsive sexual behaviour, kleptomania, compulsive shopping, food, exercise addiction, internet addiction

Food Addiction

Ø Food addiction - mesolimbic DA pathway

l Food = natural reward - palatable foods activate reward system reliably and strongly

l Homeostatic feeding + reward circuit (mesolimibic DA pathway) integrated

l regulate feeding behaviour (Leigh & Morris, 2018)

Reward circuitry in obesity - Chronic overeating

l energy requirements exceeded

l one of many factors that may explain development of obesity (Leigh & Morris, 2018)

l availability & exposure to palatable, energy dense foods

l increased stress exposure

Ø Possible alterations in reward circuit - increased activation

l governs hedonic feeding - motivated by rewarding properties of palatable foods

Ø Hedonic qualities of food – overeating

l Weak homeostatic signals

Homeostatic mechinsm between brain and GI are weak and can easily be broken down