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16. Neuroscience Exam 2 > 6. EAA and Excitotoxicity > Flashcards

6. EAA and Excitotoxicity Flashcards

1
Q

EAA stands for excitatory amino acids, what are the two main EAAs?

A

glutamate and aspartate

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2
Q

EAAs are located throughout the CNS. NMDA receptors (N-methyl-D-aspartate is exogenous). EAAs can activate the receptor leading to?

A

influx of calcium

***MODULATED by glycine

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3
Q

What is needed to bind to the NMDA receptor in order for the influx of Ca to occur?

A

both glycine and EAA

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4
Q

What is within the NMDA receptor and blocks the channel at resting membrane potential, not allowing the passage of Calcium?

A

Mg

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5
Q

becuase of the Mg in the NMDA receptor, this makes the NMDA receptor for EAAs what kind?

A

ionotropic ligand AND voltage gated

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6
Q

Within the NMDA receptor, there is also a PCP binding site which what binds and does what?

A

horse tranquilizer (PCP) binds and blocks the channel and influx of Ca

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7
Q

The non-NMDA receptors are ionotropic as well but primary have an influx of what?

A

Na

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8
Q

The AMPA receptors when bound by EAAs or exogenous AMPA will allow the influx of what, leading to what?

A

Na, and an EPSP

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9
Q

What would benzodiazepines cause if the bound to the non-NMDA AMPA receptor?

A

reduces the amount of sodium that enters

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10
Q

Kainate receptors are the second type of non-NMDA receptors which allows the influx of what when EAAs bind?

A

Na and SOME Ca

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11
Q

Non-NMDA receptors produce an EPSP with short onset/duration while NMDA receptors produce what?

A

long EPSP with long duration because lots of Ca influx and Mg in the way

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12
Q

What is the mechanism for how NMDA receptors depolrize in order to displace the Mg blocking the channel so Ca can come inside?

A

BOTH non and NMDA receptors are on the postsynaptic membrane and are both activated by EAA. Non NMDA opens and Na comes in, causing depolarization and Ca is able to enter NMDA channel

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13
Q

The functions of non-NMDA receptors are primary sensory afferents and upper motoneurons. What about NMDA receptor functions?

A

CRITICAL in short/long term memory formation

synaptic plasticity

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14
Q

EAA also have metabotropic receptors which are divided into 3 groups, which are coupled with what G protein?

A

Group 1: Gq

Group 2/3: Gi

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15
Q

Metabotropic receptors for EAAs exist pre and post synaptically, presynaptically for control of NT release and postsynaptically for? (3)

A

learning memory and motor systems

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16
Q

To limit the actions of EAAs, glial cells nearby the synaptic cleft will do what?

A

Take up the EAAs and make them into Glutamine (LIKE GABA

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17
Q

Once glutamine is made from EAA in the glial cell, what will occur?

A

Glutamine is taken back up into the presynaptic neuron and stored as EAA (?)

18
Q

EAAs will bind to NMDA on the postsynaptic neuron and allow the influx of Ca, which binds what, activating what?

A

Ca binds Calcineurin, leading to activation of NO synthase

19
Q

When Nitric Oxide synthase is activated from activation of calcineurin, what occurs within the postsynaptic neuron?

A

Arginine is made in NO and citrulline via NOS

20
Q

The production of NO from arginine, will migrate into the presynaptic neuron since it is very lipid soluble and do what?

A

increase the release of NTs

21
Q

What are two of the main functions of NO?

A

Memory in hippocampus and cerebellum

Cardiovascular and respiratory control in pons/medulla

22
Q

What is a non-neural function of NO?

A

Macrophages release NO for vasodilation

23
Q

What are three major downsides to NO?

A

very unstable w 1/2life of 5 seconds
produces free radicals
toxic to neurons in high [ ]

24
Q 
EAAs
Location:
Functions:
Ionotropic Receptors:
Metabotropic Receptors:
Other:
A 
Location: Widespread
Functions: Excitatory NT
Ionotropic Receptors: AMPA/Kainate/NMDA-R
Metabotropic Receptors: 3 groups 
Other: NMDA creates NO
25
Q

Excitoxitcity has two main players known as?

A

Calcium (NMDA Receptors)

Oxygen

26
Q

What occurs after ischemia in the brain and is responsible for damage to neurons whether or not they were exposed to the ischemia?

A

Over-stimulation of the EAA system

27
Q

During a stroke, in a localized part of the brain, blood flow stops to that region. After 4 minutes O2 reaches 0, mT stop producing ATP which leads to?

A

Na/K ATPase stops working cause no ATP, leading to depolarization of neuronal cell membrane

28
Q

Once the neuronal cell membrane is depolarized, what will happen, which usually happens when cells depolarize?

A

APs occur

29
Q

Once action potentials reach the presynaptic terminal NTs are released! (like normal except this is due to lack of O2 and blood) Strokes occur in the cortex so what NT is most likely released in mass amounts?

A

EAAs! which are released into other parts of the brain

30
Q

Ok but we’re fine right? cause we have the glial cells which take up EAAs and make them into glutamine. WRONG: what happens in this situation?

A

The uptake of EAA are dependent on ATP, which there is none of = increase of EAA/overstimulation

31
Q

The excess EAAs binds to the non-NMDAs which removed Mg from NMDA receptors allowing what?

A

large influx of Ca into post-synaptic cell = high intracellular [Ca]

32
Q

When there are high levels of calcium within a cell, what occurs?

A

Phospholipase A2 activity increases, which acts to release arachidonic acid from membrane = physical damage to membrane

33
Q

Due to the release of arachidonic acid from the membrane that PLA chewed into, it becomes a secondary messenger and INCREASE Ca release from Er and mT. Causing WHAT? (3)

A

ER stops making protein
eIF2a-kinase activation (phosphorylation)
mT dysfunction

34
Q

High levels of Ca in the cell also leads to activation of u-calpain (proteolytic enzyme). Which does what?

A

Lysis of structural proteins and eIF4G = Metabolic and Structural impairment of neurons

35
Q

With the increased numbers of Ca inside the cell, calcineurin will be activated, which activates NOS, which makes NO which will make what?

A

Free radicals (BAD) and vasodilate leading to swelling and tonsillar herniation

36
Q

As a consequence of all of the steps due to high Ca, in particular release of Ca from intracellular stores, causes mT death leading to?

A

ACTIVATION of the apoptotic pathway

mT releasese cytochrome C and caspase 9 activating caspase 3 which kills neurons everywhere cause excess EAAs

37
Q

After ischemia, reprerfusion of O2 to the areas would be good… but the changes that occured do not allow it. Why is O2 bad after ischemia?

A

mT are dead, so cannot utilize O2, so O2 becomes free radicals

38
Q

Some mT may be able to use O2 to make ATP, however there are ‘bad’ proteins activated as compared to health ones, such as?

A

PLA, calpain, calcineurin etc

39
Q

Kinases (bad cells there d/t ischemia) take the ATP and make ADP and PO4, this phosphorylations leads to?

A

PO4+ eIF2a kinase leads to FURTHER decrease in protein synthesis and further activates caspase 3 and apoptic signaling

40
Q

What is the difference between ionotropic and metabotropic receptors?

A

Ionotropic: transport ions
Metabotropic: G coupled receptor

16. Neuroscience Exam 2 (17 decks)

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