Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PMCOL 305 > 4-DA and glu > Flashcards

4-DA and glu Flashcards

1
Q

when given Ritalin, did people with lots of D2 receptors or little D2 receptors react pleasantly to the experience?

A

low levels of D2 causes euphoria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

when given Ritalin, did people with lots of D2 receptors or little D2 receptors react negatively to the experience?

A

high levels of D2 causes dysphoria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what levels of D2 receptors may be protective against addiction?

A

high levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how can you naturally increase D2 receptor levels?

A

exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what does social stress do to D2 receptor levels?

A

decrease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

where are D2 receptors most affected in the brain?

A

nucleus accumbens (that is where you feel pleasure due to dopamine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what G protein do D1 receptors use?

A

Gs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what G protein do D2 receptors use?

A

Gi/Go

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the 3 steps in Gs pathway?

A

adenylyl cyclase stimulated, increases cAMP levels, activates kinases to phosphorylate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the 3 steps in Gi pathway?

A

inhibit adenylyl cyclase, inhibit Ca+ channels, activates potassium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what does the activation of potassium channels do to neuronal firing (Gi)?

A

decreases probability that neuron will fire

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

where are D1 receptors

A

on postsynaptic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

where are D2 receptors

A

on presynaptic and postsynaptic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what does D1 receptors do to neurotransmission(excitatory or inhibitory)?

A

excitatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what does D2 receptors do to neurotransmission(excitatory or inhibitory)?

A

inhibitory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what kind of pathways are associated to D1 type receptors

A

reward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what kind of pathways are associated to D2 type receptors

A

aversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is D1 affinity to dopamine and at what concentrations

A

low affinity (only active at high concentrations)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is D2 affinity to dopamine and at what concentrations

A

high affinity (1000X higher, active at much lower dopamine concentrations)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

love who?

A

FROG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

which dopamine receptors respond to tonic levels of dopamine

A

D2 (D1 cant, it needs high concentrations)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

which dopamine receptors respond to high levels of dopamine (bursts)

A

D1`

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

if D1 and D2 receptors have different effects, why doesn’t dopamine cancel itself out when it activates the receptors?

A

they are found on different neuronal populations that form different pathways (reward vs. punishment)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what 3 things happen once D2 receptors are activated

A

1-increase K+ channel and decrease Ca++ channel (hyperpolarization)
2-increase DAT
3-inhibits TH enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is TH enzyme and what does it do

A

tyrosine hydroxylase which helps synthesis DA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is DAT

A

dopamine transporter (brings it inside the presynaptic neuron from the cleft

27
Q

why does D2 decrease Ca++ channel

A

because you need Ca++ to release NT from vesicles

AND it helps make the neuron more negative (hyperpolarized)

28
Q

why does low D2 cause a predisposition to likelyhood of addiction

A

because D2 are autoreceptors that help inhibit further dopamine release

29
Q

what happens when you knock out D2 receptors in mice and then give them cocaine

A

they become more sensitive to cocaine

30
Q

which type of neurons are D2 receptors on

A

the majority aren’t on DA releasing neurons

31
Q

how can D2 receptors affect glutamate release

A

because there are D2 receptors on glutamate releasing neurons, so if there is DA released and leaks out near another D2 receptor, it can inhibit glutamate release

32
Q

how can communication between diff. parts of the brain via glu or GABA be affected by DA? (ex:PFC communicating with amygdala)

A

DA influences the DA or GABA releasing neurons if they have D2 receptors on it, so it influences the excitability of the striatum

33
Q

how is dopamine release and expectation related

A

they are related because expectation drives the response-dopamine release can change (even with the same dose) depending on the expectations

34
Q

how would DA be released if the animal was given a dose smaller than expected

A

small - they ANGY (shuts down activity of neuron)

35
Q

how would DA be released if the animal was given a dose larger than expected

A

big - they HAPI

36
Q

what did the picture and dose experiment teach us about DA

A

not only reward, but also works with anticipation (and comparison of reward received to what was expected)

37
Q

what is the dopamine signalling in pre-reward caused by

A

due to learned behaviour from cues and expectations (like a pic associated to a dose)

38
Q

what is the dopamine signalling in post-reward caused by

A

summation of pharmacological properties of drug and expectation

39
Q

what is the role of glutamate in the brain (associated to how drugs affect the brain)

A

neuroplasticity, over-learning of behaviours and relapse

40
Q

what does glutamate signalling do to drug-related behaviours

A

it may “lock in” some of the behaviours

41
Q

where are 2 locations that glutamate is released

A

presynaptic terminals and glial cells

42
Q

where does/what causes the phasic/acute level of glutamate release

A

presynaptic terminals

43
Q

where does/what causes the tonic/basal level of glutamate release

A

glial cells

44
Q

what are mGluR (simple definition)

A

presynaptic metabotropic glutamate receptors

45
Q

what activates mGluR

A

glutamate release from glial cells

46
Q

what is the role of mGluR cells

A

to control sympathetic glutamate release (make sure there isnt excess release)

47
Q

what does the cystine-glutamate exchanger do

A

releases (approx. 60%) glutamate from the glial cells

48
Q

What does chronic drug use do to TONIC glutamate release

A

reduce it

49
Q

how does chronic drug use reduce the level of tonic glutamate release

A

inhibits the cystine-glutamate exchanger (decreases activation of presynaptic glutamate autoreceptors)

50
Q

why is more glutamate released during stress/ cue/drug stuff?

A

because cystine-glutamate exchanger is inhibited, which decreases activation of presynaptic glu autoreceptors, which turns off negative feedbacl

51
Q

what does excess glu do to the brain (2)

A

induces neuroplasticity and impairs communication between the PFC and nucleus accumbens

52
Q

what happens when both dopamine and glutamate are released on neurons in the nucleus accumbens

A

(ERK!) change in gene expression causing structure and function of neurons to change

53
Q

what is ERK stand for

A

extracellular signal-related kinase

54
Q

what causes the activation of ERK

A

only activated when dopamine and glutamate are released simultaneously on a signal neuron

55
Q

what does activation of ERK cause

A

changes in neuronal structure and proliferation

-long term changes

56
Q

where does ERK activation happen

A

postsynaptic side of a neuron, like the spiny neuron that receives both DA and glu input

57
Q

what are the steps in the ERK pathway(4)

A
  • D1 activation leads to stimulation of glu receptor
  • D1 causes adenylyl cyclase and cAMP (Gs)
  • glu causes increase Ca2+
  • ERK gets phosphorylated and can cause gene transcription (only happens if BOTH DA and glu pathways are activated)
58
Q

can ERK happen if D1 is activated but not NMDA

A

no

59
Q

is ERK activation increased or decreased with most drugs of abuse

A

increased

60
Q

what is a key role of ERK when it comes to drug abuse

A

neuronal plasticity

61
Q

what NT plays a role in transient neuroplasticity

A

dopamine

62
Q

what NT plays a role in stable neuroplasticity

A

glutamate and dopamine

63
Q

what is stable neuroplasticity

A

when your brain has already changed-it is very hard to turn back the effects of drugs

64
Q

how can you turn around compulsive relapse

A

behavioural intervention and pharmacology

-abstinence may not be enough

PMCOL 305 (26 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions