umich psych 230 exam 1

What happens when the neurotransmitter release and the neurotransmitter binds to receptors on the postsynaptic side? What do we call the postsynaptic side?

-Neurotransmitter binds to receptor.

-Receptor is activated.

-Like a key and lock mechanism
(A specific receptor will be open , with only a specific neurotransmitters or A specific neurotransmitter(e.g glutamate) can open multiple locks, different receptors. )

The postsynaptic side is called: Receptor to be "Activated" -Once it's bound to a neurotransmitter it's activated it induces the action it usually does on the post synaptic side.

-Those action include opening ion channels and Sending a G-protein coupled receptors into the nucleus.

When a specific molecule binds successfully, it's called ?

Ligand- molecule that binds to receptor.
( Some drugs can mimic what the neurotransmitter would do, by binding to the receptor, which would be consider a ligand even through they NOT innate neurotransmitter would normally bind to them)

What is a neurotransmitter?

the body's chemical messengers. They are the molecules used by the nervous system to transmit messages between neurons, or from neurons to muscles. Communication between two neurons happens in the synaptic cleft (the small gap between the synapses of neurons).

What is Glutamate?

-The most common neurotransmitter in the nervous system. It is found throughout the brain.
(i.e glutamate receptors induce depolarization following NT binding).
-Excitatory, induces EPSP on the postsynaptic side. .
-Most common ionotropic receptors are AMPA and NMDA receptors. Glutamate causes AMPA receptors to immediately open and close, while the NMDA receptors are harder to open but once open, they cause long lasting effects on the synapse by releasing additional ions.

-NMDA receptors are related to learning and memory. Also metabotropic receptors.
-90% of synapses are glutamatergic synapses

What is GABA?

Gamma Amino Butyric Acid

-Most common Inhibitory neurotransmitter found throughout the brain (causes IPSPs opposite of Glutamate).

-Opens Cl-(chloride channel), which causes hyperpolarization on the postsynaptic side. (Cl- into the cell) or K+ (K+ ions out of the cell) channels.
-Two receptors are: GABAa and GABAb

Monoamines

dopamine, epinephrine, norepinephrine, serotonin, melatonin

What are catecholamines?

A family consisting of Adrenaline (epinephrine), Noradrenaline (norepinephrine), & Dopamine, they all have the similar molecular structure.
They can be EPSP and IPSP.

(E.g Dopamine: Would induce excitation or depolarization on the postsynaptic. In other synapses, depending on the receptor on the postsynaptic, it may actually induce an inhibitory effect)

What is epinephrine and Norepinephrine?

-Also called Adrenaline and Noradrenaline
.
-General function:
Mobilize brain and body for action (fight or flight); (How do they mediate these effects in the brain and in the body) increasing arousal, increasing attention.

-Act as both neurotransmitters and hormones

-Act on different body organs: increase respiration, blood flow to muscles, pupil dilation, release of glucose (energy).

-Lowest levels during sleep, least levels of arousal and attention.

-We react to a dangerous situation because of signaling between these two neurotransmitters.

What separates Epinephrine and Norepinephrine from Glutamate and GABA, but is common with ACh?

They produced in small structures, widespread effect.
( The way these neurotransmitter act they are produced by these small neurons that can have axons that project very broadly, neurons themselves that have epinephrine and norepinephrine they have few and centralized small nuclei.)

Where does adrenaline or Epinephrine produce in?

Adrenaline produced in adrenal glands and medulla

Where does Noradrenaline or norepinephrine produce in?

Noradenaline produced in the brain in the Locus Coeruleus, and outside the brain in ganglia, skin and adrenal glands.
(The glands will receive a neural signal from the brain and then that will cause release of these hormones locally. )

If they are released by a gland into the blood stream, and via the bloodstream reaches some target organ, then we call these ?

Hormones, hormonal effect.
Fro Epinephrine and Norepinephrine, as , most neurotransmitter remain in the brain but these acts centrally and peripherally.

What is acetylcholine (ACh)?

-ACh is the neurotransmitter at the neuromuscular junction synapses between motor neurons and muscle fiber.

-A neurotransmitter found both in the brain and the PNS. Usually causes EPSPs.The neurotransmitter inside the brain, causes attention, sensation, action, learning, and locomotion/movement.

Second role: In the PNS(Peripheral Nervous System , activates the parasympathetic nervous system and peripheral motor neurons.

-The neurotransmitter that allows neural signals to act on muscles. Directly onto muscle fibers and the muscles themselves have receptors for ACh.

What is the locus coeruleus?

Locus Coeruleus: Involved in Stress, attention, noradrenaline.
Where we have many neurons that produce or synthesize and release noradrenaline to very dispersed other brain areas.

What is the special brainstem nuclei and structures?

Locus coeruleus:stress, attention, noradrenaline
Raphe Nuclei: arousal, pain, serotonin,
Superior colliculus: vision
Inferior colliculus: hearing
Ventral tegmental area: (VTA)dopamine, motivation, arousal
Substantia Nigra: movement

What is Dopamine( a catecholamine)?

Known neurotransmitter, involved in many different kinds of brain functions including movement( Substantia Nigra/death of dopaminergic neurons in Parkinson's disease)
-movement, reward-seeking, motivation, addiction.

What are the two key brain areas Dopamine is produced in? Which neurons express the neurotransmitter itself?

Substantial Nigra, and Ventral tegmental area (VTA)
They send their axons very widely to many areas.

Which neurons have receptor for the dopamine ?

We can find receptors everywhere, if we have a random neuron in the cortex it might a receptor for dopamine. It can be influenced by release dopamine coming from the VTA. Itself does not produce dopamine.or release dopamine.

A number of kinds of receptors for every neurotransmitter? How many receptors for dopamine?

Two families of dopamine receptors: D1 and D2 to which the dopamine can bind. The have differential roles. Different locks open with the same key.

What is Serotonin (5-HT)? What are some additional facts?

-Known as "happiness neurotransmitter" (not that simple, sleep, appetite,….)
-Antidepressant drugs, increase serotonin
-Produced in the Raphe Nuclei
-Mixed EPSP and IPSP effect it can induce excitation and induce inhibition.

What are opioids?

-Endorphin and Enkephalin
-Called the natural morphine" ( comes from the opium poppy mimics that activity of the endorphins and enkephalins in out body in regular natural conditions)
-Pain reduction, reward, euphoria.
-Negative consequences: heroin
iced EPSP's and IPSPs
-Bind to opioid receptors
-Synthesized following pain, exercise, laughter

-The opium poppy makes us feel relaxed and euphoric, but we don't know exactly how. Some say if a substance from the poppy can do this, there must be receptors in our brain for it. And if those receptors exist, our body probably makes its own substances that can also activate them.
But why would our body have receptors for these substances? It seems strange unless our body naturally produces something similar that can activate these receptors. That's what we mean by an intrinsic ligand—a natural substance our body makes to activate these receptors.

Natural or synthetic morphine-like substances responsible for reducing moderate to severe pain

What is Reverse Neurotransmitter? Nitric Oxide

-Soluble gas (NO) in dendrites
-different then other neurotransmitter oppositely.
(generated by postsynaptic enzyme in response to neurotransmitter)
-Leaks out of dendrite
-The nitric oxide is releases by the postsynaptic side as a results of a lot of neurotransmitter binding. (Backwards) Normally it's the presynaptic side binding to the postsynaptic side.

-Enters presynaptic neuron without any membrane receptors because its a gas.
-Retrograde signaling; Think of nitric oxide (NO) like a messenger that can travel backward in the brain. When there's a lot of neurotransmitter released in a synapse (the gap between two brain cells), NO can travel back to the cell that released the neurotransmitter. When it gets back there, it tells the cell to either release more or less of that neurotransmitter. So, it's like a feedback system—it helps to control how much of a neurotransmitter is floating around, making sure everything stays balanced and working smoothly in the brain. This helps with learning, memory, and other brain functions.

• Influences presynaptic mechanisms of neurotransmission
• Feedback
  (Stop 27:40)

Amino Acid Neurotransmitters

GABA and glutamate

Peptide neurotransmitters

endorphins, enkephalins, somatostatin, cholecystokinin

Gas neurotransmitter

nitric oxide, carbon dioxide

Organic cation neurotransmitter

acetylcholine

AMPA receptors

weak stimulation activates receptors, and they cause a slight depolarization of the post synaptic neuron

NMDA receptors

strong stimulation causes release of Mg2+ ion that usually blocks NMDA channels. Once the Mg2+ is released, Na+ and Ca2+ are released. The increase in Na+ causes more Na+ to enter existing AMPA receptors AND causes new AMPA receptors to arrive at surface of post synaptic neuron

ACh pathway in the brain

ACh is found in the nucleus basalis and septal nuclei. These areas then send out projections to the rest of brain.

ACh at neuromuscular junction

ACh is found at the synapse between a motor neuron and a muscle fiber

Sarin

Toxic chemical weapon. An inhibitor of acetylcholinesterase which is normally an ACh degrader. It causes ACh buildup and prevents muscle relaxation which causes involuntary movement and complete loss of control of bodily functions.

Norepinephrine

Both EPSP and IPSP. General function is to mobilize the brain and body for action. Active in the sympathetic autonomic system (fight or flight). Produced in the locus coeruleus which is most important for stress and attention.

Dopamine

Both EPSP and IPSP. Produced in the substantia nigra and ventral tegmental area. Active in movement, reward, and motivation. Lack of dopamine known to cause Parkinson's disease.

Serotonin

Mixed EPSPs and IPSPs. Known as the happiness neurotransmitter but also important sleep and appetite. Produced in the raphe nuclei. Commonly seen with antidepressant as they increase serotonin.

Opioids

Mixed EPSPs and IPSPs. Endorphins and Enkephalins. known for pain reduction, reward, euphoria, relaxation. They bind to opioid receptors, and they are the body's natural morphine. They are synthesized following pain and exercise, and studies have shown even after laughter.

Nitric Oxide

Gas released by post-synaptic enzyme in response to neurotransmitter. Leaks out of dendrite and enters the presynaptic neuron. NO doesn't need membrane receptors as it penetrates the membrane directly. Activates presynaptic second message…type of feedback.

Each neurotransmitter has lots of receptors

multiple locks

Agonists

drugs that increase the action of a neurotransmitter. Presynaptic: release NT
Postsynaptic: activate receptor

Antagonist

drugs that turn OFF the NT system
Presynaptic: prevent release
Postsynaptic: block receptors

inverse agonist

chemical substance that produces effects opposite those of a particular neurotransmitter in postsynaptic neuron

L-Dopa (presynaptic agonist)

is a dopamine precursor. Given to patients with Parkinson's because they have reduced dopamine levels. We must give them L-Dopa instead of straight dopamine because dopamine cannot cross the blood-brain barrier.

Cocaine (presynaptic agonist)

inhibits the reuptake of dopamine (and serotonin and norepinephrine) by blocking dopamine transporters. This increases the latency of dopamine to stay in the synaptic cleft.

Amphetamines (presynaptic agonist)

more extreme version of cocaine. blocks and reverses dopamine transporter. increases levels of dopamine and norepinephrine. causes stimulation, euphoria, wakefulness, improved cognitive control. Sometimes used for the treatment of ADHD, narcolepsy, depression, and an athletic performance enhancer

SSRIs (presynaptic agonist)

block the reuptake of serotonin and increase the serotonin in synapse. commonly prescribed antidepressant is prozac.

Morphine and Heroin (postsynaptic agonist)

Activate postsynaptic opioid receptors and cause euphoria and pain relief. mimic endorphins and enkephalins. synthetic opioids include fentanyl and carfentanyl.

LSD (postsynaptic agonist)

hallucinogenic drug that activates serotonin receptors

Benzodiazepines (postsynaptic agonist)

examples include Xanax and Valium. Cause sedative, hypnotic, anti-anxiety, anti-epileptic effects. Also used as a muscle relaxant. Benzo's bind to GABA receptors and facilitate GABA effects causing a reduction of neural activity. Benzos make the channels more permeable with GABA to Cl- for an enhanced effect.

Antipsychotics (postsynaptic antagonists)

for schizophrenia, block D2 dopamine receptors and prevent dopamine from activating. atypical antipsychotics block serotonin receptors but can also block dopamine receptors

Receptor down-regulation

Process by which some receptors decrease in number meaning there are fewer receptors to activate resulting in a tolerance to the drug. Also results in a withdrawal in the absence where the normal neurotransmitter gives a normal signal--> this kind of deficit can lead to relapse but not always.

neural sensitization

Neurons become hyper sensitive to a drug. Work by UofM labs and dopamine sensitization and addiction with wanting v liking.

Neurotoxicity

cell death and damage to the nervous system by a toxic substance

psychophysics

how the quantitative aspects of physical stimuli correlate with the sensations they evoke, measures perception

sensory coding

how the quantitative aspects of physical stimuli correlate with the neural activity with evoke. receptor neurons convert sensory stimuli into neural signals

electrophysiological recording

Measure of the electrical activity across the membrane of a nerve cell by use of electrodes. Extracellular recording places the electrode outside but nearby the cell of interest; intracellular recording places the electrode is placed inside the cell of interest.

optical recording of action potentials

calcium sensitive dyes are used in two photon calcium imaging

raster plot

A graphic representation of occurrences in a certain temporal relation.

rate code

information coded by spike rate

temporal code

information coded by spike timing

somatosensory homunculus

Broad areas of primary somatosensory cortex devoted to particular body regions

cortical plasticity

the capacity to change cortical organization as a result of experience, ex: training monkeys to perform tasks using tips of fingers or phantom limbs in humans

phantom limb

perceived sensation, following amputation of a limb, that the limb still exists because part of brain that used to function for limb that is gone is now taken over by other modalities

Mike May

blinded by a chemical explosion at 3. He had scarring of the cornea that blocked light, underwent surgery that cleared corneas but was still unable to see. The brain pathways that interpret visual information from the eyes were not functioning. After years of training, he regained partial vision…we don't see with only our eyes.

Mach Band illusion

Each band is consistent across is width, but it looks darker on the left and lighter on the right than it does in the middle

The first action potential occurs in the visual pathway occurs in the…

retinal ganglion cell

phototransduction

light strikes a light-absorbing pigment molecule, rhodopsin, in the disc of a photoreceptor. Rhodopsin breaks down into opsin and retinal. Opsin closes Na+ gates and hyperpolarizes the photoreceptor. This stops glutamate release and inhibits some bipolar cells and excites some others. This causes depolarizations/hyperpolarizations to be sent on to ganglion cells.

Rods

Specialized visual receptors that play a key role in night vision and peripheral vision.

Cones

retinal receptor cells that are concentrated near the center of the retina and that function in daylight or in well-lit conditions. The cones detect fine detail and give rise to color sensations.

color blindness

lack of one or more cone pigments

fovea

the central focal point in the retina, around which the eye's cones cluster--> here is where the highest density of cones and few rods are. non-photoreceptor cells are pushed aside here.

On center - off suround

light in center excites, light in surround inhibits

off center on surround

light in center inhibits, light in surround excites

Spots at intersection

white intersection inhibited by 4 white sides, white bars inhibited by only 2 sides, so the intersections are darkened by the extra inhibition. less darkness in surround do will fire less, therefore we perceive junctions as darker.

On center bipolar cells

reverse signal sent by photoreceptors

The Mach band illusion is a result of

lateral inhibition occurs, the cell at the edge is influenced by darkness right next to it so that's why we perceive it to be brighter while the cell in the middle does not fire too much

bionic retina

works when photoreceptors are damaged. RCGs are electrically stimulated by microprocessor. Not best or most clear vision.

The blind spot of the eye is

where the optic nerve exits the back of the eye

each retina is divided into:

nasal and temporal hemiretina; the projections diverge at the optic chiasm

nasal hemiretina cross over and cause:

the left visual field is represented in our right hemisphere and vice versa…NOT right/left eye but visual field

LGC axons go to…

Lateral Geniculate Nucleus (LGN)

layers 1 and 2 of LGN (Magnocellular)

motion and dim light sensitive (from rods)

Layers 3-6 of LGN

color and detail resolution (from cones)

LGN receptive fields

like retinal ganglion cells, they are on center-off surround. they have bigger receptive fields than ganglion cells, they can see larger chunk of visual space

The axons from the LGN go to the part of the brain called

primary visual cortex (V1)

Primary Visual Cortex (V1)

1. each V1 neuron responds to a stimulus in a small area in the field of view
2. neighboring V1 neurons respond to stimuli in nearby locations in the visual field

maintains retinotopic organization

from LGN to V1

thalamus (LGN) projects directly to layer 4

Hubel and Wiesel

studied feature detection in visual cortex and discovered simple, complex, and hypercomplex cells

simple cells

Cells in V1 that respond to line, or gradient, oriented in particular direction

complex cells

V1 cells that respond to a line in a specific angle at any location--> more generalizing

how do we get responses to oriented lines in V1 from responses to spots in the LGN?

cortical ring compression

lesions in V1

patients report partial or complete blindness to single or both hemispheres. when asked to detect objects, they appear blind. When humans are forced to guess or use vision, they do well--> blindsight
people perceive blindness but they actually have access to visual info (but they are not aware).

Patient TN

lost V1 in both hemispheres due to stroke. ordinary vision tests indicated complete blindness. researchers asked him to walk down a corridor where they had placed obstacles without his cane, and he avoided obstacles smoothly.

what does blindsight teach us?

primary visual cortex is critical for the conscious aspects of vision. Vision still goes through primary visual pathways like retina and thalamus but information is enough to guess

from V1 to V2

neurons in V2 respond to visual illusions while V1 does not. V2 neurons are closer to our visual perception

ventral stream

what stream, what is being seen. responds to increasingly complex stimuli.

dorsal stream

where stream, where things are, movement & location in space

V4

responds to complex geometric shapes, and is the first area in the ventral stream to show attention modulation

ventral what stream

Parvocellular LGN neurons --> V1 --> V2--> V4--> Inferior Temporal Lobe (IT)

Inferior Temporal Lobe

responds to visual objects in a position invariant and size invariant manner

fusiform face area (FFA)

area within IT that responds to faces. here is where detecting and differentiating between faces is very important.

controversy behind the FFA

car experts and bird experts show increased activity in FFA when shown their object of expertise