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Flashcards in Ch 11 maybe Deck (30):
0

Gs pathway makes this

protein kinase a (PKA) from cAMP

1

four cAMP bind to blank regulatory subunits

two

2

two regulatory subunits liberates two blank subunits

catalytic

3

catalytic subunits blank other blank

phosphorylate, proteins

4

PKA blank to the nucleus, and phosphorylates blank

translocates, transcription factors

5

transcription factors turn on blank

gene expression

6

very well known transcription factor

creb

7

creb activates very important blank for things like blank and blank

genes, eating/moving, drug addictions/sympathetic nervous system

8

this hormone increases ATI gene expression

aldosterone

9

ATI receptors are blank receptors and are an example of influencing transcription factors to influence blank

metabotropic, behavior

10

this promotes thirst

angiotensin

11

increased receptor blank leads to increased blank of angiotensin 2

expression, effectiveness

12

this pathway works the same as Gs, but it inhibits blank so blank is not produced

Gi, adenylyl cyclase, cAMP

13

tough pathway

Gq

14

Gq pathway

1. PIP breaks into two
2. IP3 and DAG come from PIP
3. DAG activates PKC in the cell membrane
4. IP3 liberates intracellular calcium

15

calcium released by ip3 binds to blank

calmodulin

16

calmodulin complex binds to blank of the dependent protein kinase

regulatory domain

17

PKC can do what action

open/close ion channels

18

arachidonic acid leads to the production of

prostaglandins

19

what produces prostaglandins that is produced by arachidonic acid

cyclooxygenase

20

tyrosine kinase receptors steps

1.signal binds
2. dimer forms
3. phosphorylated by atp
4. activates relay proteins leading to a response

21

mapk pathway

1. ras
2. raf
3. MEK
4. MAPK
5. Transcription factors

22

retrograde signaling activates enzymes and increases blank

nt reelease

23

when the postsynaptic cell releases NO which travels to presynaptic cell to stimulate increased nt release

retrograde signaling

24

in the presynaptic terminal, second messengers can regulate blank

nt release

25

in the postsynaptic neuron, second messengers can regulate blank

postsynaptic potentials

26

in the soma second messengers can regulate blank and blank

resting potential, ap dynamics

27

pka opens ion channels through blank

phosphorylation

28

pka also activates blank which causes the ion to blank

inhibitor 1, stay open

29

mapk can be activated through g protein coupled receptors, which is blank of the g protein

independent