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NS-1 > EAA and Excitoxicity > Flashcards

EAA and Excitoxicity Flashcards

1
Q

Where does aspartate serve as a neurotransmitter?

A

visual cortex and pyramidal cells

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2
Q

What are the receptor types for EAA?

A

ionotropic and metabotropic

several kinds of each

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3
Q

What is the NMDA receptor?

A

EAAs activate it –> influx of calcium

has multiple modulatory sites - glycine binding site

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4
Q

How does glycine affect the NMDA receptor?

A

required co-agonist, but it alone cannot open the channel

both EAA and glycine must be present for the channel to open

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5
Q

How does magnesium affect the NMDA receptor?

A

within the channel itself

blocks the channel at resting membrane potential

prevents Ca influx when the channel opens

makes the receptor both ligand and voltage-gated

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6
Q

How does PCP affect the NMDA receptor?

A

blocks channel

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7
Q

What are the 2 main types of non-NMDA receptors for EAA?

A

AMPA

Kainate

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8
Q

What is AMPA?

A

non-NMDA receptor for EAA

ionotropic - primarily Na influx

glutamate/aspartate are the endogenous ligands

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9
Q

What is the main regulatory site for AMPA?

A

benzodiazepines bind site on extracellular face of protein

reduce the amt of sodium that enters

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10
Q

What is the difference in excitation from activation of non-NMDA and NMDA receptors?

A

non-NMDA: typical excitatory post-synaptic potential (epsp)

NMDA: long latency epsp w/ long duration

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11
Q

Why does NMDA receptor have a longer latency epsp?

A

non-nmda receptor act –> typical epsp –> depolarization can cause Mg to leave NMDA channel –> Ca now enters NMDA channel –> longer lasting epsp

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12
Q

What is the relationship based on location of non-NMDA and NMDA receptors?

A

non-NMDA receptors do not exist on post-synaptic membranes w/out NMDA receptors

in some systems

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13
Q

What are the functions of EAA receptors?

A

non-nmda: primary sensory afferents, upper motoneurons, others

nmda: critical in short and long-term memory formation, synaptic plasticity

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14
Q

What are the main groups of metabotropic EAA receptors and what is their GPCR type?

A

group 1: Gq

Groups 2 and 3: Gi

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15
Q

Where are EAA metabotropic receptors and what do they function in?

A

pre-synaptic: control NT release

post-synaptic: learning, memory, motor systems

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16
Q

How are EAAs broken down and how does this limit EAA actions?

A

glial cells surrounding synapses absorb EAA –> breakdown to glutamine = inactive

glutamine uptaken to presyn neuron and recycled to EAA

17
Q

How are NMDA receptors and nitric oxide related?

A

EAA binds NMDA –> Ca influx –> binds calcineurin

NOS triggered to convert Arginine to NO

18
Q

Influx of what ion is likely to cause an inhibitory post-syn potential (ipsp)?

A

chloride

19
Q

What type of NT is glycine typically?

A

inhibitory

20
Q

What is the main effect of EAA at NMDA receptors?

A

producing long-term changes in synaptic strength via a process known as long term potentiation

memory

learning

21
Q

Which receptor is thought to be used with EAA for synaptic plasticity assoc w/ learning?

A

metabotropic receptors

22
Q

What are the general effects of NO outside CNS?

A

increases cGMP in endothelial cells –> causes sm m relaxation

major inhibitory NT in gut –> relaxation

immune: free radial in macrophages to kill bacteria

23
Q

What are the CNS effects of NO?

A

long term potentiation of presyn neuron (respiratory control, cardio control, memory/learning)

*major control of cerebral vasculature –> dilation

24
Q

How is NO removed from a synapse?

A

no uptake system for NO as it is lipid soluble

half-life of 5 seconds and then it degrades

some proteins do bind it

25
Q

What occurs to neuronal cells right after ischemia?

A

rapid reduction in ATP –> cell depolarizes as membrane ATPases stop working –> presyn cells release NTs –> excess activation of NMDA and non-NMDA receptors

26
Q

How is the excess activation of EAA receptors further promoted during ischemia?

A

reuptake of EAA is dependent on Na concetration gradient

w/ energy depletion, gradient for Na degrades –> no reuptake –> a ton in the synapse

27
Q

What happens to cells after ischemia causes excess EAA activation?

A

calcium enters cells –> voltage gated Ca channels open too

activation of phopholipase A and C, Calcineurin, and mu-calpain

28
Q

What does the activation of phopholipases following an ischemic event cause?

A

act on cell membrane to release arachidonate from membrane –> physical damage

arachidonate –> ER and Mitochondria release calcium –> ER shows ulfolded protein response and ER kinases are activated

29
Q

What does is mu-calpain?

A

a protease activated in ischemia –> damages structural and functional proteins within the cell

inhibits protein synthesis

30
Q

What does release of calcium from the ER do to mitochondria?

A

mito membrane is disrupted –> cytochrome c and caspase 9 released –> caspase 3 –> apoptosis

31
Q

What does oxygen do to damaged neurons during reperfusion?

A

taken into cells –> mitochondria make ATP

leftover O2 made into peroxide radicals –> peroxidation of lipids and membrane damage

elF2alpha kinase Piates elF2alpha –> inhibts protein synthesis and activates caspase 3 and CHOP –> apoptosis

32
Q

How does epinephrine from ischemic injury damage cells?

A

able to get to tissue after reperfusion –> Beta receptors –> cAMP –> increased extracellular K and activates PKA –> more protein syn inhibition

33
Q

What does ischemia do to endothelial cells lining blood vessels?

A

causes them to express cell adhesion molecules so WBCs can enter –> macrophages –> release NO and Histamine

34
Q

How are ischemia and growth factors related?

A

ischemia impairs cells’ ability to respond to GFs bc of:

membrane damage

altered fxn of sendary messenger sys

inhibition of protein synthesis

35
Q

What does increased blood flow during reperfusion do to the brain?

A

increase of vascular permeability bc of a ton of NO –> influx of fluid in damaged areas –> edema –> increased ICP –> compromizes blood flow to areas

36
Q

What enzyme is directly responsible for structural damage to neurons during excitotoxicity?

A

mu-calpain

NS-1 (50 decks)

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