Neuro Final

Attention definition

state of selectively processing simultaneous sources of information

no multi-tasking- only shifting and dividing attention

attending to something

enhances visual detection and has widespread areas throughout the brain

various sensory areas= Area V1, visual cortical areas in the parietal and temporal lobes

target detection

valid cues- detection and accuracy rises

invalid cues- detection drops, draws attention away

neutral cue- baseline, does not draw attention but can tell its there

reaction time

valid cues- react faster, lower reaction time

invalid cues- slow reaction, higher reaction time

neutral cues- ex: see an exit sign that isn’t yours

Neglect Syndrome

associated with right-sided lesions = left side of body/objects does not exist

left hemisphere attends to right side BUT right hemisphere attends to both

Functional MRI

something in visual area=located on visual sector

sector changes in different areas of retina= different areas of brain is stimulated/brain activity shifts depending on where in the central vision

Retinotopy= different areas of retina light up different parts of brain

Selective vs Divided attention

Selective- one feature, detection rate is good, ex: click button when see blue

Divided- all features, accuracy goes down and time goes up ex: click when see a blue square and moving L to R

color and shape

V4- big part of visual cortex that goes into parietal

Inferior tegmental area (IT)- association area

other areas in the temporal lobe

speed and motion

medial tegmental area (MT)

attention has different sources

green (fast), blue (color), orange (shape)

injuries can cause deficits but can be different aspects depending

Facial blindness

Oliver Sacks- see face but cannot identify, facial recognition area responds to faces

neural plasticity= use unusual features to identify a person

Parietal cortex

helps identify things

assumption: attention changes location prior to eye movement (something interesting causes us to look)

looking at fixation point/saccade

posterior parietal cortex- normally lights up randomly - but when target turns on (valid) activity bursts/ invalid= not a lot of activity. Helps us recognize what we want to see

V4- lights up/ becomes active with valid response

intraparietal cortex- important in directing eye movement

V4 and cues

sees valid cue, activates = connect memories to it

connects memory, sight, and eye direction

Pulvinar Nucleus

back of thalamus → divides and guides attention to multiple areas of brain

GABA shuts nucleus down and makes it hard to guide attention

ADHD

lower activity/cortical function in cortex- inhibitory system is not properly working

medications increase cortical activity

Frontal Eye Field (FEF)

eyes move to attended objects in the environment

neurons direct our view and eye to things that are interesting : V4 lights up and can identify/connect to memories

have to inhibit the reaction (staring or reacting in public)

FEF stimulation: mimics physiological and behavioral effects of attention

neurology vs psychiatry

neurology- physiological process that drive behavior (drugs change function of brain)

psychiatry- thought process that go into behavior, talk therapy

2 theories of mental illness

Freud- mental illness- unconscious and conscious elements of the psyche come into conflict

Skinner- many behaviors and learned; repeat successful behaviors because had previous success in that approach

Syphilis and mental health

general paresis of the insane - people started getting manic and go through a cognitive deterioration (looks like rapid Alzheimers)

started the thought that mental illnesses have direct biological causes (mind + body connection)

Anxiety disorders

inappropriate expression of fear to something that should not be fear inducing

Common anxiety disorders

Panic disorder- sudden fear without stimulus

Agoraphobia- fear of being outside; needs isolation of social context

OCD- thoughts of the obscene or forbidden; intrusive thoughts

GAD- sympathetic all times; no sleep, digestion problems

Specific phobias- fear is out of proportion of specific stimulus

Social phobia- fear of interacting w people in large groups

PTSD- sympathetic quickly; brain shrinks, triggering memmories

stressors and stress response

stressors- fear evoked by a threatening stimulus / manifested by the stress response - can be strengthened or weakened based on experience

HPA axis (hypothalamic pituitary adrenal axis)- CRH and ACTH release cortisol

hypothalamus → CRH released → anterior pituitary gland → ACTH → adrenal gland releases cortisol

Amygdala and Hippocampus

both regulate CRH neurons

Amygdala- activates the HPA axis

Hippocampus- deactivates the HPA axis - Glucocorticoid receptors hit the inhibitory loop to CRH to turn it off

Treatments for anxiety disorders

psychotherapy/psychosocial- occupation based activities- assist in anxiety rising occupations

Anxiolytic (anti-anxiety) meds

Benzodiazepines- bind GABA channels, forces Chlorine channels to take in more GABA so it makes more inhibitory transmission

SSRI- block uptake of serotonin to allow more serotonin in the active zone

All drugs target CRH receptors

Affective disorders

physical sign of mood - referred to as mood disorders

disorders of the diffuse neurotransmitter systems (norepinephrine, serotonin)

Major depression

Depression- inability to feel happy things

Dysthymia- milder form

Bipolar disorder

manic-depressive disorder: depression + mania

mania: hyperactive, hypersexual, poor judgement

hypomania: slightly elevated by not as bad

Monoamine Hypothesis

problems with diffuse modulatory system (norepinephrine and serotonin)

depending on where the medicine is affected - depends on what will happen to the product

drugs and what they do with mood disorders

Tricyclics: block the reuptake of norepinephrine and serotonin

MAOI: stop breakdown of neurotransmitter (norepinephrine and serotonin)

Fluoxetine: SSRI stops breakdown of only serotonin

diathesis stress hypothesis

genetics is how big the cup is and water is how much stress / water spills= show stress response

treatments for affective disorders

Electroconvulsive therapy (ECT)- localized electrical stimulation that changes the way neurons connect, targets the temporal lobe, quick relief

Can have preemptive memory loss (black before ECT) and postnatal memory loss (cant create new memories after)

Lithium

treatement for affective disorder (es bipolar) : heavy metal that slows down secondary messenger by going into sodium channels

slows down/eliminate mania and depression

takes time to be effective, has a sweet spot; too much wont help and will increase side effects; tardive dyskinesia (involuntary movement of lips and jaw, permanent)

Schizophrenia

loss of contact with reality, hallucinations, strong genetic tie, ventricles enlarge and loss of neurons

Paranoid- everyone is out to get you

Disorganized (more common)- cannot integrate in society well, unhoused population - talking to nobody, hear voices

Catatonic- complete separation of the psyche from the body

Hypothesis of schizophrenia

Dopamine- too much dopamine in the prefrontal area of brain; start hallucinating and showing psychotic side effects; want to decrease the amount of available glutamate for those in a psychotic episode

Glutamate- taking acid and inhibit glutamate in some receptors and excite glutamate in others / fast excitatory in the AMPA and NMDA receptors can excite connections

PCP- no pain compliance because psychosis disassociates them from pain

Treatments for schizophrenia

drug therapy combined with psychosocial support

haloperidol- commonly prescribed- works with D2 receptors decreases the positive symptoms of schizophrenia- has numerous side effects

Also reduces NMDA to attack the NMDA receptors if they are responding to glutamate

Cell proliferation

start at ventricular → marginal zone → pial surface

1st position- extend the cellular process to the field surface, retract the process to pull the neuron up towards pial surface

2^nd position- migrates all to pial surface and DNA cell gets copied

3^rd- 2 complete copies of the gene and goes down to ventricular surface

4th- cell retracts that arm from the pial surface = cell division

vertical vs horizontal cleavage

everytime a cell divides it goes through vertical or horizontal

vertical- 2 cells side by side : split notch and numb and will be identical and stay in ventricular zone

horizontal- notch and nub separated - numb is in ventricular zone and notch goes to pial surface to become part of the cortex

Pyramidal cells and astrocytes

notch that travels up (vertically) and horizontal

happen first

Inhibitory interneurons and oligodendroglia

sideways, along the ventricular zone - stay down

inside out way of developing

migrate neurons up into cortex

first to arrive become layer 6 (deepest)

2^nd set is layer 5

3^rd, 4^th layer, and the last to populate will be the first of the 6 layers of the pyramidal cells

Layer 6 -> to layer 1 populate

cell differentiation

once cell gets to where it goes it takes on the characteristics of a neuron

neuroblast -> put out processes -> exposed to something- gets repulsed or attracted

draws the dendrites towards another object or neuron that is producing the substance -> axons are repulsed so lead away from it = nice mature differentiated neuron that is communicating with something else

Don’t want axon to be drawn towards previous neuron so it can go somewhere else

Protomap

protomap helps guides the way they populate

Neurons that are alike agitate together and make a nucleus - radial glial guides the neurons at different times

Happens because of the thalamus - it coordinates the protomap

three phases of pathway formation

(1) pathway- neurons travel along and make a pathway - growing trajectory of the neuron

(2) target- leaves the neuronal bodies to aggregate at the LGN (can be diff things) - start to differentiate and send synapses

(3) address- make diff parts of the lateral geniculate nucleus their home - where they are going to set up and the layers

Growing axon

growth cone is tip of the neurite

axons are connected together with cell adhesion molecules – so all axons terminate in a similar place

Extracellular matrix- cells adhere and move along it – draw axons to the next set of addresses (pulls axon to destination)

Pioneer axons

Pathways get set before the brain has expanded too much – pioneer axons are set and stretch as nervous system expands

Pioneer axons provide guidance for where the neurons are going to end up - send out growth cones to connect

contact guidance- something is sticky; sticks and allows to travel down

contact Inhibition-something repulsive and pulls back

Synaptogenesis

connecting mature axons with target

Growth cone coming down from axon – bumps into muscular junction – releases agrin molecules- musculienrigic receptor- receptor creates rapsyn (pulls ach from other parts of neuronal membrane) – migrate and create a neuromuscular junction

agrin molecules cause a reaction that reinforces the connection between neurons

Synaptic stabilization

too many synapses made that could ever be used (overproduction)

“Pruning”, a process of neuronal death- competitive process

experience dependent changes

Synapse formation

Philapodium reaches out, make contact and synaptic vesicles migrate and send neurotransmitters to the area, release proteins that attract surface proteins (receptors) = active zone

presynaptic postsynaptic relationship

competition for troping factors

troping factors= neurotransmitters, proteins on the surface, electrical gradients, nerve growth

input neurons (more of these) connect to target neurons if available - if no connection is available cell death

Apoptosis: Programmed Cell Death

synaptic elimination

at neuromuscular junction: each synapse has to choose its best function

Alpha motor neuron sends message to sarcomere, as the body moves and develops (motor selective) - will pull back the synapses to the muscle fibers that don’t respod as efficiently - the ones that do respond will make the connections

Synaptic convergence

basis of binocular vision and binocular receptive field

both eyes overlap and can see things well

monocular deprivation

damage an eye (or covered) = the neurons that are associated with the open eye live and specialize- will get more neurons that have repurposed themselves from the eye that no longer exists

Critical period for plasticity

early for sight and goes down over the youth of the child

injured during critical period= have easier time compensating for the loss / up to bout 9 years of age the ability to change and repurpose neurons is very high

end because= plasticity diminishes, axon growth ceases, stop trying to make synapses with other neurons

inhibitory circuitry is the last to develop (GABA)

Two rules for synaptic modification

1: neurons that fire together wire together - Hebbian modification

2: out of sync lose their link (prune back)

glutamate receptors

Differences in the type of transmission they do - both cause depolarization

AMPARs: glutamate-gated ion channels: accepts glutamate and allows sodium in (no Ca)

NMDARs: glutamate comes out and kicks out Mg which allows Ca2+ and Na to come in - Calcium reinforces the connection between the presynaptic and postsynaptic neuron

Long-Term Potentiation

long term NMDA receptor - system has learned something and has a permanent relationship - memory

NMDA is activated it causes AMPLIfication- increases the amount of signaling and causes synapses to split and double and reinforces the connection

Long-Term Synaptic Depression (LTD) 

neurons fire out of sync - opposite of long term potentiation

binding sites starts getting drawn away - lose the receptor binding sites - decreases the amount of activity in the AMPAS

Learning vs memory

learning- acquisition of new information

memory- retention of learned information

Declarative vs nondeclarative memory

can transfer from one to another from experience =

declarative- facts and events; medial temporal lobe and diencephalon

nondeclarative- procedural memory, skills, habits (riding a bike or playing an instrument); in the striatum

Classical conditioning- emotional responses and motor memory

Amnesia

common side effect of neurological dysfunction serious loss of memory and/ability to learn

limited- bound in time to when the injury happened- forget before and after

dissociated- no other cognitive deficit

Retrograde vs anterograde amnesia

Retrograde- forget things you already knew before injury

Anterograde- inability to form new memories - interrupt short and long term after injury

Transient global amensia

ischemia (swelling in brain)- causes permanent memory gap- shorter and temporary- disoriented, ask same questions repeatedly

norepinephrine- increases the plasticity and decrease the chance of apoptosis

Lashley maze learning

we need areas to produce memories, our memories are distributed widely throughout the brain - so destroying the cortex can destroy parts of our memory

Hebb and Cell Assembly

Stimulus -> activates neurons in different areas –(temporary electrical relationship) -> neurons keep reverberating (sending same signal over and over) – basis of short term and working memory

If you continue to think about they strengthen connections -> conformational changes in the proteins of communicating neurons (fire together wire together) – create their own proteins at synaptic level that create permanent relationships→ long term memory

electrically connected (short term) → physically connected (long term)

Inferotemporal (IT)

declarative memory - lights up when first seeing people

IT- lesion = will cause problems with visual tasks- this area helps trigger our memory for faces

communicates with facial recognition area and located in the medial temporal lobe

Temporal lobe

remembers specific memories and draws memories from parts of the cortex (auditory cortex, physical memory) also essential to understanding learning and memory

Lobotomy = every day resets, inability to create new declarative memories but he remembers anything that happened before (nondeclarative was still present)

Removal of temporal lobes had no effect on perception, intelligence, personality

Declarative memory

Information flow : circuit will reinforce until it distributes and create permanent relationships

When you repeat many times you consolidate the memory- go from short term to long term declarative memory

Sleep needs to happen for consolidation

Diencephalon

associated with memory and lesion= amnesia

important in memory processing

declarative memory

Hippocampus

only active when triggering/retrieving memories

lesion= do not have an organized way of finding food, make lots of errors when going down radial arms (rats)

Korsakoff’s Syndrome

long term alcoholism –thiamine deficiency- causes different lesions to appear – confused, make up memories, abnormal eye movement, tremors / give thiamin to not reverse the problem but it doesn’t get worse

Place cells

how we help to locate different places in the environment -we end up orienting because of NMDA receptors changes in the hippocampus

Morris water maze- uses glutamate receptors for place cells / take an animal that has a temporal lobe lesion= cannot find stand

Procedural memory

Disrupt Caudate Putamen = no procedural memory

striatum

becomes a habit not a memory (tying shoes)

habit learning is different based on disease (amnesia vs parkinson’s)

Working memory

most recent memories try to shove in brain - have a large frontal lobe -self-awareness, capacity for planning and problem solving

stuff we need to do (close eyes are can grab cup because you know where it is)

goes from medial temporal to different directions –

keep a lot of memory in bottom route – gives a reverberating circuit (hebb’s circle) that allows to remember something

Top direction- cingulate cortex where you keep memories

Prefrontal area

working memories spans the whole prefrontal and frontal lobe

Striatum

damaged= procedural memory is damaged but not declarative memory

damage striatum= double dissociation