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Neuro 223 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

what is a neuron?

A

a cell that detects and responds to stimuli to send information over a long distance

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2
Q

what is a neuroglia?

A

it is a cell that protects, repairs, and assists neurons

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3
Q

what was the original 1839 cell theory?

A

that all organisms are composed of one or more cell, the cells are the basic units of structure, and all cells arise from pre-existing cells

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4
Q

(disproven) what was the reticular theory?

A

that all nerve cells were connected and formed a continuous network

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5
Q

what is a unipolar cell

A

one who’s dendrites and axons come out of one side of the cell body, the dendrites eventually separating from the axon

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6
Q

what is a bipolar cell

A

a cell who has two ends, one side has an axon, one side has a dendrite

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7
Q

what is a pseudo-unipolar cell

A

where the cell body comes off the side of the axon, where the axon goes in both directions, and on one end the axon becomes a dendrite

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8
Q

what is a multipolar cell?

A

where an axon comes out of one side, and dendrites come out from all kinds of directions

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9
Q

afferent vs. efferent

A

afferent: info towards the brain (sensory neurons)
efferent: info away from the brain (motor neurons)

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10
Q

neural circuits
(convergent excitation, divergent excitation, feedforward excitation, feedback excitation, recurrent (lateral) excitation, lateral inhibition, disinhibition)

A

write out and check against image in review

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11
Q

how does a knee jerk reaction work?

A
  1. a mallet hits the knee
  2. the extensor muscle sends a signal to the brain via the sensory afferent neuron
  3. the sensory neuron sends excitatory messages to an inhibitory interneuron which inhibits the efferent flexor motor neuron, but it sends excitatory messages to the efferent extensor muscle neuron
  4. this causes the leg to swing forwardw
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12
Q

what is an oligodendrocyte?

A

it facilitates greater conduction across axons, especially between the nodes of ranviar by myelinating axons

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13
Q

what is a schwann cell?

A

it is the oligodendrocyte of the peripheral nervous system, and does the same thing but not in the central nervous system

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14
Q

what is a microglia?

A

an immune cell that removes damage and debris (macrophage)

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15
Q

what is an astrocyte?

A

they regulate the BBB and create strong K+ buffering, promoting synapse formation

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16
Q

what are glial stem cells?

A

cells that give rise to new glial neurons

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17
Q

what are types of electrical signals that can give rise to an action potential?

A

external stimulation (light, sound, pressure, etc.) – usually for sensory neurons

chemical stimulation (via neurotransmitters)

strong stimulation

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18
Q

what is voltage?

A

the difference in electrical charge between two places
(usually in reference to across a membrane)

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19
Q

what is current

A

the rate of flow of charged particles

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20
Q

what is resistance

A

the opposition to flow of charged particles

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21
Q

what can’t pass through a phospholipid bilayer?

A

polar molecules without active transport

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22
Q

how is the resting potential established and maintained at a neuron membrane?

A

ATPase pump, leak cells are equal in and out when at electrochemical equilibrium

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23
Q

what is the Nernst equation?

A

Eion = (58/z) log([x]out/[x]in)

z = the charge of the ion
[x] = ion concentration

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24
Q

what is the Goldman equation?

A

Vm = (Pk[K]out + Pna[Na]out + Pcl[Cl]in) / (Pk[K]in + Pna[Na]in + Pcl[Cl]out)

Pk = the permeability of that ion across the membrane

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25
Q

what is electrochemical equilibrium?

A

a balance between the concentration gradient that makes an ion want to diffuse across the membrane and the electrical gradient that stops the ion from leaving the cell

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26
Q

how to prove that increased permeability is responsible for the depolarization of the membrane?

A

put a neuron in a solution with varying levels of Na+ concentration

RESULT: find that the spike height of the action potential depends on how high the external Na+ concentration is

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27
Q

how does Ohm’s law explain the rush of Na+ ions into a cell during an action potential?

A

Ohm’s law is voltage = current * resistance

resistance is the inverse of conductance (which is just permeability) –> so permeability is the inverse of resistance

Therefore,
current = voltage * permeability

I(ion) = g(ion) * (Vm - E(ion))

g is conductance, I is current

so the rate that Na+ flows across the membrane is a product of its membrane permeability and electrochemical driving force

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28
Q

the sequence of an action potential

A
  1. Na+ ions enter the cell, causing it to depolarize
  2. voltage-gated ion channels open, causing Na+ to flood in
  3. the depolarization moves across the axon, and as it moves the voltage-gated sodium channels close and the K+ channels open (these channels stay open for longer, causing overshoot)
  4. all channels are closed and RMP is reestablished

*K+ channels are slower

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29
Q

how does the voltage clamp method work?

A

it shows the current required to hold a certain voltage (holds the membrane at a certain voltage and see how the cell responds)

when its held at highly positive voltages, there’s a high moment of Na+ conductance and longer increased concentrations of K+

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30
Q

which are faster, ion channels or active transporters?

A

ion channels, bc diffusing down concentration gradient. Ion channels are passive

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31
Q

why must active transporters always be working to maintain the membrane voltage?

A
  1. has to go back to normal after neural signaling
  2. there is continual leakage at rest, need ATPase pumps to respond accordingly
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32
Q

what are the gating mechanisms of ion channels?

A
  1. ligand gated
  2. temperature dependent
  3. g-protein signaling
  4. voltage gated
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33
Q

what is distinct at the structure of a Cl channel?

A

its a dimer (two molecules linked together) with two pores

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34
Q

how many genes are in each channel of a Na+, Ca2+, K+ and Cl- ion?

A

Na+, Ca2+, and K+ all have four

Cl- has two

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35
Q

what is cell-attached recording?

A

what: tight contact between pipette and membrane

use: allows accurate measurement of the current flowing through one of a few channels in the patch, can even sometimes just look at a single channel

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36
Q

what is whole cell recording?

A

what: tears a hole in membrane, where the cytoplasm is continuous with pipette interior (has strong suction to keep it in place)

use: allows the voltage of the cell to be measured of controlled

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37
Q

what is inside-out recording?

A

what: cuts a piece of membrane off at two points, exposes it to air

use: makes the inside cytoplasmic domain accessible, can see how the outside of the cell responds via pipette

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38
Q

what is outside-out recording?

A

what: tears off membrane at two points, then reattaches where the inside is facing the inside of the pipette

use: makes the extracellular domain accessible, can see how the inside of the cell responds via pipette

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39
Q

when will a voltage-gated ion channel open?

A

its more likely to open at higher voltages, but its also a probability

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40
Q

how does the selectivity filter select for K+ ions in K+ channels?

A

K+ ions are dehydrated when they pass through the filter and are pushed through by electrostatic repulsion

4 protein loops around poor line the walls, carbonyl groups on the poor interact with the unsolvated K+ ion, balancing energy requried to remove its hydration cell

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41
Q

why couldn’t a sodium ion travel through a K+ channel?

A

its too small and t/f energetically unfavorable

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42
Q

stages of a sodium channel

A
  1. closed
  2. open
  3. inactivating
  4. inactivated
  5. closed

*important note, it inactivates while the voltage is still depolarized, bc refactory period

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43
Q

how does the inactivation of the Na+ channel work?

A
  1. only 3 of the 4 sensing domains are required to open the Na+ channel
  2. the fourth Na+ channel is the slowest one and is tied to inactivation of the channel
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44
Q

why does the K+ channel take longer to open than the Na+ channel?

A

it requires all four voltage sensing domains to be activated, while Na+ only requires three

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45
Q

what are channelopathies?

A

neurological disease caused by altered ion channels

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46
Q

what is ataxia?

A

the loss of voluntary motor movement, caused by altered K+ channels and Ca2+ channels

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47
Q

what is optogenetics?

A

manipulating neural activity via light
- ChR2, NpHR, Arch

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48
Q

benefits of optogenetics

A

bidirectional (can hyperpolarize and depolarize)

ex. yellow light is inhibitory

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49
Q

what is the difference between a chemical and electrical synapse?

A

a chemical synapse is slower and the ap is spread to the postsynaptic neuron via neurotransmitters, whereas an electrical synapse is much faster and activated via connexon channels (a type of ion channel at the gap junction)

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50
Q

what is one of the few CNS spaces that utilizes electrical synapses?

A

hippocampal interneurons

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51
Q

connexon
- # subunits
- how it allows molecules to cross

A
  • 6 subunits
  • passive flow through gap junction, large pores that allow ions, ATP, and second messengers
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52
Q

general sequence of events at a chemical synapse

A
  1. neurotransmitters stored in vesicles
  2. an action potential invades the synaptic cleft
  3. the depolarization opens Ca2+ voltage-gated channels
  4. the invasion of Ca2+ causes the vesicles to fuse with the membrane
  5. neurotransmitters are released into the synaptic cleft via exocytosis
  6. the neurotransmitters send inhibitory or excitatory signals to post synaptic neuron
  7. neurotransmitters are reuptaken by a glial cell or by enzymatic degragation
  8. retrieval of vesicular membrane from plasma membrane
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53
Q

what is an end plate potential?

A

a chemically induced change in electrical voltage measured at the neuromuscular junction. an electrode is inserted at the endplate to see how the release of neurotransmitters at the presynaptic neuron affecs the postsynaptic neuron depolarization/ hyperpolarization

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54
Q

how did we discover that chemical transmission was a thing?

A
  1. heart experiment: put a heart in a solution and stimulated the vagus nerve electrically, whatever was around that heart went to another heart and caused the rate of beats to slow down, proving that there’s a physical substance excreted by the neurons (later discovered as acetylcholine)
  2. did electrophysical pictures that showed neurotransmitters in vesicle pockets
  3. recorded end plate potential of frog neuromuscular junction, found that stimulating the axon led to a post synaptic membrane potential, when the EPP exceeded threshold
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55
Q

proving MEPP occur spontaneously

A

when a cell is in a Ca2+ deprived bath, still have MEPP recorded, showing that its spontaneous

56
Q

what is the relationship between a MEPP and EPP?

A

there is a direct 1:1 relationship, showing that a postsynaptic cell is directly stimulated via neurotransmitter vesicles (organized in quantals)

STUDY: following the stimulus by low Ca2+, the distribution of EPP is consistent with amplitudes of MEPP’s

57
Q

why do we know that Ca2+ entry is required for transmitter release?

A

STUDY:
control (w Ca2+) vs. Ca2+ channel blocker

when the blocker is in place (cadmium), there is no post-synaptic membrane potential

in the control (with Na+ and K+ channels blocked, a depolarizing post-synaptic membrane potential is still recorded)

58
Q

why is Ca2+ necessary and sufficient?

A

proved that it affects the postsynaptic potential

proved that in the absence of Ca2+ there is no postsynaptic potential

59
Q

small molecule neurotransmitter vs. large dense core vesicles

A

small molecules are in small clear-core vesicles and only require low frequency stimulations and localized increase in Ca2+ concentration

large dense neuropeptide vesicles require high frequency stimulation and a more diffuse increase in Ca2+ concentration

60
Q

what does SNARE proteins do?

A

SNARE is SNap REceptor

they help the vesicle dock and form a complex that sits the vesicle on the membrane

the complex is made of synaptobrevin, syntaxin, and SNAP-25

61
Q

what does Synaptotagmin do?

A

entering Ca2+ binds to synaptotagmin that hands off the vesicle, leading to curvature of the membrane to bring them together

–> fusion of the membrane leads to exocytotic release of neurotransmitter

62
Q

what are synapsins for?

A

holds the reserve pool together in preparation of release to membrane

what would happen without synapsin: vesicles wouldn’t be ready for release, unable to transfer ap across cleft, more improbably system

63
Q

what is CaMKII for?

A

phosphorylates synapsin to help move vesicles from release poll to docking

what would happen without CaMKII: vesicles would be stuck in the reserve pool

64
Q

what is syntaxin for?

A

is on the membrane, binds with synaptobrevin on the vesicle to faciliate docking

what would happen without syntaxin: vesicles couldn’t dock on membrane and release neurotransmitters

65
Q

what does clathrin do?

A

coats membrane to allow for curvature, facilitating dynamin-induced separation of the membrane to replenish vesicles

what would happen without it: there would be insufficient replenishment of vesicles, bc couldn’t pull them from membrane

66
Q

what does dynamin do?

A

constricts the neck of the membrane to replenish vesicle supply

what would happen without it: there would be insufficient replenishment of vesicles, bc couldn’t pull them from membrane

67
Q

what does synaptobrevin do?

A

part of SNARE complex that facilitates docking

what would happen without synaptobrevin: the vesicle wouldn’t be able to dock and thus release neurotransmitters into membrane

68
Q

which are t-SNARE?

A

syntaxin and SNAP-25

69
Q

which are v-SNARE

A

Synaptobrevin

70
Q

how does BoTX affect neurotransmitter release?

A

they cleave either SNAP-25, syntaxin, or synaptobrevin

(something about the docking/ releasing complex)

71
Q

theories of endocytosis

A

“kiss and run” barely opens and closes again

clathrin mediated

bulk retrieval, only during high frequency release

72
Q

what causes the end plate potential?

A

the opening of ligand-gated acetylcholine receptors

73
Q

does the postsynaptic membrane potential affect the end plate current?

A

when the post synaptic potential is negative, an EPC makes it more negative, whereas when its positive, after a certain point the current reverses direction back to 0

this demonstrates the reverse potential

the action of a neurotransmitter drives the postsynaptic membrane potential towards Erev for the particular ion channel being activated

74
Q

how to utilize Ohm’s law to find the reversal potential?

A

EPC = g * (Vm - Erev)

when EPC is 0, changes direction

g = ionic conductance of molecule

Erev = electrochemical driving force

75
Q

when does the molecule have an outward and inward current on an amplitude graph of Erev?

A

above 0 its a strong outward current and below 0 is a strong inward current

76
Q

is membrane potential the same thing as voltage?

A

yes

77
Q

how does Erev of a particular ion affect the postsynaptic potential?

A

based on the potential of the postsynaptic neuron, the voltage is either driven up or down by the released ions, as they drive towards their Erev levels

78
Q

when is a neurotransmitter excitatory?

A

when the channel being driven releases ions who’s Erev is above threshold

*a current that brings the PSMP to be more positive can still be inhibitory if its reversal potential is still below threshold

79
Q

how do peptide neurotransmitters reach the synapse?

A

they’re synthesized in the cell body and transported via axonal transport

80
Q

how are small-molecule transmitters synthesized?

A

enzymes for synapse are synthesized in the cell body and transported via axonal transport, synthesis happens at nerve terminals

81
Q

what are ionotrophic receptors?

A

ligand-gated ion channels

82
Q

what are metabotrophic receptors?

A

g-protein coupled receptor

83
Q

GABA

A

category: amino acid

impact: inhibitory

receptors: ionotrophic (5 subunits), structure similar to nAcHRs

synthesis: formed from glumatate, removed from cleft by GABA transporter (GAT), VGAT facilitates entry into vesicles

where: local circuit interneurons

84
Q

GABAaR

A
  • structure: similar to nAChRs, heteropentameric
  • inhibitory bc permeable to Cl- who’s Erev is below threshold
  • too much GABA: coma
  • too little GABA: seizures
  • associated diseases: anxiety, mood disorders, epilepsy
85
Q

glycine

A

category: amino acid

impact: inhibitory

receptors: ionotrophic

where: local circuit interneurons

86
Q

glutamate

A

category: amino acid

impact: excitatory

other facts: nearly all excitatory neurons in the CNS are glutamatergic, does not cross BBB

receptors: ionotrophic (4 subunits), metabotrophic (7 subunits)

synthesis: glutamine synthesized with glutaminase locally at presynaptic terminals

87
Q

glutamate receptors

A

(ionotrophic) AMPARs:
- large, fast EPSC (excitatory post synaptic current)
- permeable to Na+, K+
- ligand-binding domain is a “clamshell” that shuts and moves gate helices to open channel when glutamate is attached
- 4 subunits

(ionotrophic) NMDARs:
- slower EPSCs and last longer
- permeable to Ca2+ too
- also voltage gated by Mg2+, and when the membrane is depolarized Mg2+ moves from blocking the channel
- co-incident detector: ligand and voltage gated
- 4 subunits

(metabotrophic) glutamate receptors:
- 3 classes with varying physiological roles
- implicated in synaptic depression of mGluR signaling affecting Alzheimer’s disease
- venus flydrap domain inactive when glumatate not bound

88
Q

what are biogenic amines?

A

synthesized from aa by removal of carboxyl group

89
Q

serotonin (5HT)

A

category: biogenic amine

impact: sleep, wakefulness, emotions

associated disease: depression, anxiety, schizophrenia, ESPECIALLY psychosis

receptors: ionotrophic, metabotrophic (7 subunits)

90
Q

histamine

A

category: biogenic amine

impact: (CNS) arousal and attention, (PNS) allergic response and inplammation

receptors: 4 types of metabotrophic receptors

91
Q

dopamine

A

category: biogenic amine

impact: coordinate body movements

associated disease: drug abuse w motivation and reward, cocaine inhibit transport (DAT), loss of coordination-Parkinson’s, dopamine agonists treat schizophrenia, bd, psychosis

location: VTA/ NA

receptors: metabotrophic (7 subunits)

92
Q

norepinephrine (noradrenaline)

A

category: biogenic amine

impact: attention, arousal, wakefulness, fight/ flight response (PNS)

location: CNS, locus coeruleus

receptors: metabotrophic (beta and alpha adrenergic receptors)

93
Q

acetylcholine

A

Category: acetylcholine

Structure: acetyl CoA & choline

Release: neuromuscular junction

impact: excites skeletal muscles, inhibits cardiac muscles

Other facts: used as Alzheimer’s meds, promotes wakefulness

exocytosis: enters vesicles via VAChT

synthesis: broken down by acetylcholinerase in postsynaptic terminal, reuptake of choline via ChT, binds with acetyl in cell via choline acetyltransferase

94
Q

acetylcholine receptor

A

nAChRs (ionotrophic)
- 5 subunits, 2 ACh binding sites, both in alpha and must be occupied
- gates twist leading to tilting of the transmembrane domains and causing gate to open
*wide pore, permeable to Na+ and K+

mAChRs (metabotrophic muscarinic AChR)
- 7 subunits

95
Q

what is a purine?

A

neurotransmitter’s who’s synaptic vesicles contain ATP that is co-released w the NT

*ATP acts as an excitatory nt in motor and sensory neurons

96
Q

ATP receptors

A

(ionotrophic)
- trimeric
- nonselective cation
- pain sensation

(metabotrophic)
- causes drowsiness (blocked by caffeine)

97
Q

what are neuropeptides?

A

receptors: metabotrophic

impact: pain transmission(substance P), pain suppression(endorphin, enkephalins), suppresses appetite(CCK)

where: brain, spinal cord, digestive tract, some are hormones

98
Q

what is substance P?

A

a neuropeptide
mediates pain tramsmission

99
Q

what is endorphin?

A

neuropeptide
pain suppression

100
Q

what is enkephalins?

A

neuropeptide
pain suppression

101
Q

what is CCK nt?

A

neuropeptide
suppresses appetite

102
Q

how do immature neurons vs mature neurons respond to GABA?

A

in immature neurons, GABA is excitatory because there Cl- channels are less functional so there is greater intracellular Cl- so the Erev is above threshold

there are more efficient Cl- transporters in mature neurons

103
Q

what is endocrine signaling?

A

broadcasting over a radio station
(entire body-blood/slow)

104
Q

what is paracrine signaling?

A

posting a flyer
(local effects-extracellular fluid)

105
Q

what is neuronal signaling?

A

email/ phone call
(direct/ fast effects)

106
Q

what is contact-dependent chemical signaling?

A

face-to-face conversation

107
Q

when do neurotransmitters not require a protein receptor?

A

when they are lipid soluble

108
Q

can there be signaling molecules that aren’t neurotransmitters?

A

yes, ex. gases such as nitric oxide

109
Q

what are lipid soluble molecules?

A

steroids, noepinephrine

110
Q

what is the difference between ionotrophic and metabotrophic receptors?

A

ionotrophic receptors mediate behavior as ligand gated ion channels while metabotrophic receptors modulate behavior as GPCRs

111
Q

types of g protein coupled receptors

A

(7 TMs)

signaling via protein phosphorylation:
- kinases phosphorylate ATP
- phosphorylates ATP w protein kinase

signaling via GTP-binding protein:
- GDP removed and replaced by GTP
- includes heterotrimeric and monomeric G-proteins

112
Q

Gs (stimulatory GPCR pathway)

A
  1. g-protein binds
  2. adenylyl cyclase
  3. cAMP
  4. PKA
  5. increase protein phosphorylation
113
Q

Gi (inhibitory GPCRs)

A
  1. G-protein binds
  2. inhibits adenylyl cyclase
  3. inhibits cAMP
  4. inhibits PKA
  5. decreases protein phosphorylation
114
Q

Gq GPCR’s

A
  1. phospholipase C
  2. DAG or IP3
  3. PKC or Ca2+ release
  4. increase in protein phosphorylation and activates calcium-binding proteins
115
Q

breaking down Gq pathway

A

what is phospholipase C? an enzyme that hydrolyzes lipids in the plasma membrane (IP3 and DAG)

DAG and Ca2+ phosphorylate PKC

116
Q

examples of Gs receptors

A

serotonin, histamine, beta adrenergic receptor(norepinephrine)

117
Q

examples of Gq receptors

A

mGluR

118
Q

examples of Gi receptors

A

vasopressin, 5HT1c, mAchR, Alpha2 adrenergic receptors (noepinephrine)

119
Q

G-protein cycle

A
  1. resting state, receptor not bound to ligand
  2. ligand binds to GPCR, G-protein releases GDP and acquires GTP
  3. Ga and Gby subunits separate
  4. the two units separately affect effector proteins
  5. Ga subunit hydrolyzes the GDP w GAPs and becomes inactive when its bound to GDP
  6. subunits recombine and inactivate
120
Q

how does cAMP activate PKA?

A

cAMP phosphorylates the substrates and activates cAMP

121
Q

examples of kinases (phosphorylating substances)

A

PKC, PKA, cAMP

122
Q

how does caffeine affect GPCRs?

A

increases HR, inhibits breakdown of cAMP, increases HR

– if cAMP is not broken down, it will continue to increase expression of PKA and excite

123
Q

how does nicotine affect GPCRs?

A

stimulates norepinephrine, increases HR

124
Q

how does beta blocker affect GPCRs?

A

inhibits beta 1 receptor, decreases HR

125
Q

how does Ca2+ facilitate LTD?

A

via the Gq route, release of Ca2+ stimulates PKC to downregulate AMPA receptors, inducing exocytosis from the membrane

126
Q

how does Ca2+ interact within the membrane?

A

many mechanisms to maintain low levels of Ca2+ (pumps)
- binds to calmodulin and Ca2+ and calmodulin complex activate CaMKII, a kinase, which helps it phosphorylate AMPA proteins

127
Q

how is CREM activated?

A

convergence of multiple signaling pathways
1. GPCR leading to PKA
2. Ca2+ channel creating the Ca2+/calmoduline kinase IV
3. RTK creating MAP kinase along w Ca2+ channel

this leads to phosphorylation of the CREM protein within the nucleus, leading to transcription and translation and a new protein

128
Q

what are enzyme coupled receptors?

A
  • 1 TM
  • assemble complexes
  • important in cell survival and proliferation
129
Q

how does an RTK receptor generally function?

A
  1. dimer molecule binds to RTK
  2. kinase activity is stimulated leading to phosphorylated tyrosines (active RTK)
  3. signaling proteins bind to the phosphorylated tyrosines
  4. the adaptor protein connects to a Ras activating protein which inactivates Ras by phosphorylating the attached GDP to GTP
130
Q

2 types of RTKs

A
  1. Trk receptors, which are activated by neutrophin ligands which are secreted. these are short range compared to hormones but long range compared to eprhins
  2. Eph receptors, activated by ephrin ligands, transmembrane proteins.
131
Q

3 pathways for Trk receptors

A

PI 3 kinase pathway
1. adapter protein
2. PI 3 kinase
3. Akt kinase
4. cell survival

ras pathway
1. GEF
2. ras
3. kinases
4. MAP kinase
5. neurite outgrowth and neuronal differentiation

PLC pathway
1. phospholipase C
2. IP3 or DAG
3. Ca2+ release or PKC
4. neutrite outgrowth and neuronal differentiation

132
Q

why are Trks important for cell survival?

A

when neurotrophins bind, promotes NGF (nerve growth factor) to prevent cell death

133
Q

EphB receptors

A

thought to regulate excitatory synapse development via regulation of actin polymerization

134
Q

dendritic spines?

A

where proteins are localized to concentrate signaling molecules

135
Q

what are the cell surface receptors?

A
  1. GPCRs
  2. enzyme-coupled
  3. ion channel-coupled
136
Q

how was LTP discovered?

A

1973 STUDY, found that in vivo reserach on rabbits in hippocampus found that greater stimulation altered the later response (greater ESPC)

137
Q

how is LTP molecularly formed?

A

when there is a strong influx of depolarization, at glutamatergic receptors there’s a great influx of glutamate, activating the AMPA and NMDA receptors especially, this activation leads to the downstream affects of NMDA, which is influx of Ca2+, Ca2+ binds with calmodulin and CamKII and helps transcribe more AMPA receptors

Neuro 223 (5 decks)

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