Ch 11 maybe Flashcards

0
Q

four cAMP bind to blank regulatory subunits

A

two

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1
Q

Gs pathway makes this

A

protein kinase a (PKA) from cAMP

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2
Q

two regulatory subunits liberates two blank subunits

A

catalytic

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3
Q

catalytic subunits blank other blank

A

phosphorylate, proteins

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4
Q

PKA blank to the nucleus, and phosphorylates blank

A

translocates, transcription factors

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5
Q

transcription factors turn on blank

A

gene expression

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6
Q

very well known transcription factor

A

creb

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7
Q

creb activates very important blank for things like blank and blank

A

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

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8
Q

this hormone increases ATI gene expression

A

aldosterone

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9
Q

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

A

metabotropic, behavior

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10
Q

this promotes thirst

A

angiotensin

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11
Q

increased receptor blank leads to increased blank of angiotensin 2

A

expression, effectiveness

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12
Q

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

A

Gi, adenylyl cyclase, cAMP

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13
Q

tough pathway

A

Gq

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14
Q

Gq pathway

A
  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
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15
Q

calcium released by ip3 binds to blank

A

calmodulin

16
Q

calmodulin complex binds to blank of the dependent protein kinase

A

regulatory domain

17
Q

PKC can do what action

A

open/close ion channels

18
Q

arachidonic acid leads to the production of

A

prostaglandins

19
Q

what produces prostaglandins that is produced by arachidonic acid

A

cyclooxygenase

20
Q

tyrosine kinase receptors steps

A
  1. signal binds
  2. dimer forms
  3. phosphorylated by atp
  4. activates relay proteins leading to a response
21
Q

mapk pathway

A
  1. ras
  2. raf
  3. MEK
  4. MAPK
  5. Transcription factors
22
Q

retrograde signaling activates enzymes and increases blank

A

nt reelease

23
Q

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

A

retrograde signaling

24
Q

in the presynaptic terminal, second messengers can regulate blank

A

nt release

25
Q

in the postsynaptic neuron, second messengers can regulate blank

A

postsynaptic potentials

26
Q

in the soma second messengers can regulate blank and blank

A

resting potential, ap dynamics

27
Q

pka opens ion channels through blank

A

phosphorylation

28
Q

pka also activates blank which causes the ion to blank

A

inhibitor 1, stay open

29
Q

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

A

independent