Karius Excitatory Amino Acids

Question 1

Where is glutamate made from

Answer 1

alpha-ketoglutarate

Question 2

What is aspartate made from

Answer 2

oxaloacetate

Question 3

Ionotropic receptor

Answer 3

NMDA and non-NMDA receptor

Question 4

how is NMDA activated

Answer 4

by exogenous agent NMDA

Question 5

What ion increases when NMDA is activated

Answer 5

Ca+

Question 6

What binding sites are necressary for NMDA receptors

Answer 6

NT, glycine, Mg+ and PCP

Question 7

Why is the EPSP slower for NMDA receptors

Answer 7

because of the multiple binding sites

Question 8

Can NMDA produce EPSP on it’s own

Answer 8

no it needs glycine and Mg+ binding

Question 9

Glycine binding site

Answer 9

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

Question 10

Mg+ binding site location

Answer 10

inside the channel

Question 11

How to get Mg+ out of channel

Answer 11

glycine has to depolarize the cell to open the channel first

Question 12

PCP binding site

Answer 12

irreversible binding to receptor

- even more interior than Mg+

Question 13

Function of PCP binding site

Answer 13

block the channel

Question 14

Characteristics of NMDA receptor EPSP

Answer 14

slow onset, prolonged duration

Question 15

Why does it take longer (slow onset)

Answer 15

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

Question 16

Why is it a longer duration

Answer 16

because calcium is entering and calcium is bigger than sodium

Question 17

Ion associated with non-NMDA receptors

Answer 17

sodium

Question 18

Two subtypes of non-NMDA receptors

Answer 18

AMPA and kainate

Question 19

how are the non-NMDA subtypes opened

Answer 19

by excitatory amino acids

Question 20

Binding sites on non-NMDA receptor

Answer 20

EAA/AMPA site and benzodiasepine site

Question 21

Function of benzodiazepine site

Answer 21

inhibits response to NT and decreases excitatory response

Question 22

Activation of non-NMDA receptor leads to..

Answer 22

EPSP and can be activated by itself

Question 23

NMDA vs non-NMDA receptors

Answer 23

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

Question 24

Why does NMDA need non-NMDA

Answer 24

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

Question 25

Metabotropic receptors

Answer 25

both pre and post synaptic locations

Question 26

How to get rid of Excitatory amino acids

Answer 26

uptake systems and glia

Question 27

Uptake Systems

Answer 27

Na+ dependent secondary active trasport | High affinity

Question 28

Glia

Answer 28

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

Question 29

NMDA receptors and Nitric oxide

Answer 29

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

Question 30

Neural functions of NO

Answer 30

long-term potentiation and memory and cardiovascular and respiratory control

Question 31

What happens if NO can't be turned off

Answer 31

apneusis - can't breathe

Question 32

Nitric Oxide and it's toxicity

Answer 32

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

Question 33

Overexcitability

Answer 33

causes cell death in cells that weren't ischemic before

Question 34

Excitotoxicity is involved with

Answer 34

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

Question 35

Excitotoxicity and epilepsy

Answer 35

repeated epilepsy can cause cell damage and become very severe

Question 36

Area most affected by ischemia

Answer 36

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

Question 37

What mechanics cause the cell to depolarize

Answer 37

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

Question 38

Increased Ca+ and Phospholipase A2

Answer 38

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

Question 39

Unfolded protein response

Answer 39

stops making protein

Question 40

Increased Ca+ and meu calpain

Answer 40

proteolysis occurs - breakdown of proteins that are already present

Question 41

Increased Ca+ and activation of calcineurin

Answer 41

a phosphatase that increase NOS and NO synthesis in toxic amounts

Question 42

Disruption of mitochondria and ER function with increase Ca+

Answer 42

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

Question 43

Reperfusion injury

Answer 43

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*

Question 44

Mitochondria and reperfusion injury

Answer 44

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

Question 45

Enzymes in reperfusion injury

Answer 45

enzymes activated aren't normal (kinases)

Question 46

Kinases in reperfusion injury

Answer 46

are phosphorylating things they shouldn't which increaes apoptotic signaling

Question 47

What can a high quantity of NO contribute to?

Answer 47

edema and damaging capillary endothelial cells