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COM Neuro > Karius Excitatory Amino Acids > Flashcards

Karius Excitatory Amino Acids Flashcards

1
Q

Where is glutamate made from

A

alpha-ketoglutarate

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2
Q

What is aspartate made from

A

oxaloacetate

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3
Q

Ionotropic receptor

A

NMDA and non-NMDA receptor

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4
Q

how is NMDA activated

A

by exogenous agent NMDA

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5
Q

What ion increases when NMDA is activated

A

Ca+

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6
Q

What binding sites are necressary for NMDA receptors

A

NT, glycine, Mg+ and PCP

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7
Q

Why is the EPSP slower for NMDA receptors

A

because of the multiple binding sites

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8
Q

Can NMDA produce EPSP on it’s own

A

no it needs glycine and Mg+ binding

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9
Q

Glycine binding site

A

acts as co-agonist and is required for EAA but glycine alone can’t open the channel

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10
Q

Mg+ binding site location

A

inside the channel

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11
Q

How to get Mg+ out of channel

A

glycine has to depolarize the cell to open the channel first

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12
Q

PCP binding site

A

irreversible binding to receptor

- even more interior than Mg+

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13
Q

Function of PCP binding site

A

block the channel

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14
Q

Characteristics of NMDA receptor EPSP

A

slow onset, prolonged duration

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15
Q

Why does it take longer (slow onset)

A

because the Mg++ needs to be done because only then will the EPSP start

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16
Q

Why is it a longer duration

A

because calcium is entering and calcium is bigger than sodium

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17
Q

Ion associated with non-NMDA receptors

A

sodium

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18
Q

Two subtypes of non-NMDA receptors

A

AMPA and kainate

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19
Q

how are the non-NMDA subtypes opened

A

by excitatory amino acids

20
Q

Binding sites on non-NMDA receptor

A

EAA/AMPA site and benzodiasepine site

21
Q

Function of benzodiazepine site

A

inhibits response to NT and decreases excitatory response

22
Q

Activation of non-NMDA receptor leads to..

A

EPSP and can be activated by itself

23
Q

NMDA vs non-NMDA receptors

A

can have NMDA and non-NMDA together
non-NMDA can work alone
NMDA can NOT work alone – need non-NMDA

24
Q

Why does NMDA need non-NMDA

A

non-NMDA allows sodium in and allows depolarization to move the Mg+ out of the way in the NMDA

25
Q

Metabotropic receptors

A

both pre and post synaptic locations

26
Q

How to get rid of Excitatory amino acids

A

uptake systems and glia

27
Q

Uptake Systems

A

Na+ dependent secondary active trasport

High affinity

28
Q

Glia

A

convert EAA to glutamine and glutamine can’t bind to anything so it is inactive

29
Q

NMDA receptors and Nitric oxide

A

influx of calcium which binds to calcineurin to activate nitric oxide synthase which catalyzes a reaction with arginine to make nitric oxide

30
Q

Neural functions of NO

A

long-term potentiation and memory and cardiovascular and respiratory control

31
Q

What happens if NO can’t be turned off

A

apneusis - can’t breathe

32
Q

Nitric Oxide and it’s toxicity

A

macrophages make NO and it will kill bacteria but some cells survive against it and make more NO when stressed out and the neighboring cells die

33
Q

Overexcitability

A

causes cell death in cells that weren’t ischemic before

34
Q

Excitotoxicity is involved with

A

cerebral ischemia/stroke
hypoxia or anoxia
mechanical trauma to CNA
hypoglycemia

35
Q

Excitotoxicity and epilepsy

A

repeated epilepsy can cause cell damage and become very severe

36
Q

Area most affected by ischemia

A

anoxic core – cells that will die if they are deprived of oxygen and can’t meet metaboic needs which will cause the cells to depolarize

37
Q

What mechanics cause the cell to depolarize

A

the cessation of the Na/K ATPase within 4 minutes which causes an increase is Na+ (depolarization)

38
Q

Increased Ca+ and Phospholipase A2

A

cause physical damage to membrane from enzyme chewing
cause release of calcium from intacellular store (Mitochondria and ER)
cause unfolded protein response

39
Q

Unfolded protein response

A

stops making protein

40
Q

Increased Ca+ and meu calpain

A

proteolysis occurs - breakdown of proteins that are already present

41
Q

Increased Ca+ and activation of calcineurin

A

a phosphatase that increase NOS and NO synthesis in toxic amounts

42
Q

Disruption of mitochondria and ER function with increase Ca+

A

ncrease cytoplasmic calcium which can leave to apoptotic pathway (caspases and caspase 9 and 3)

43
Q

Reperfusion injury

A

provide oxygen to cells that have been hypoxic they now don’t use the oxygen well and the oxygen ends up a free radical somewhere which is bad

44
Q

Mitochondria and reperfusion injury

A

Mitochondria try and use the ATP but don’t work because they dumped all their Ca+ and are following apoptotic pathway instead

45
Q

Enzymes in reperfusion injury

A

enzymes activated aren’t normal (kinases)

46
Q

Kinases in reperfusion injury

A

are phosphorylating things they shouldn’t which increaes apoptotic signaling

47
Q

What can a high quantity of NO contribute to?

A

edema and damaging capillary endothelial cells

COM Neuro (4 decks)

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