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BBB 270 Exam 3 Review PPT > BBB 270 Exam 3 Review PPT > Flashcards

BBB 270 Exam 3 Review PPT Flashcards

1
Q

caffeine half life

A

4 hours

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2
Q

caffeine eliminated

A

urine

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3
Q

caffeine low dose

A

stimulatory

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4
Q

caffeine high dose (3)

A

reduced activity / increased tension and anxiety

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5
Q

caffeine mechanism of action

A

Caffeine activates the dopamine system indirectly by

inhibiting Adenosine A2A receptors, which then results in an increase in D2R signaling

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6
Q

acute effects

A

Increased BP, increased respiration rate, diuresis (most prominent in non-regular
users)

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7
Q

caffeinism (1000 mg/day) is characterized by

A

high craving/withdrawal, nervous, restless, insomnia, tachycardia 


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8
Q

mild caffeine withdrawal

A

headache, fatigue, concentration impairment, mild anxiety/depression

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9
Q

therapeutic for

A

apnea, increasing analgesic properties (excedrin)

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10
Q

caffeine mechanism of action

A

partial blockade of adenosine A1 and A2A receptors (induce sleep)

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11
Q

caffeine inhibits

A

GABA A ->stimultate Ca2+ release and inhibit phosphodiesterase

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12
Q

THC affects

A

CB1 in CNS and CB2 in immune system, bone, fat, GI

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13
Q

cannabinoid receptors are all

A

metabotropic (GPCRs)

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14
Q

when THC binds GPCRs

A

inhibit AC and Ca2+ channels,

open K+ channels (hyperpolarizing)

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15
Q

THC receptors are located _ and inhibit _

A

on presynaptic cell (retrograde messengers), presynaptic neurotransmitter release

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16
Q

endogenous cannabinoids are synthesized

A

on demand and not packaged into vesicles

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17
Q

Effects of THC

A

increased blood flow to skin (flushing), increase HR, increase hunger, reduced locomotion

memory deficits (via CB1 receptor, decrease in LTP)

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18
Q

endocannabinoids are

A

retrograde messengers

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19
Q

endocannabinoids

A

AEA and 2-AG

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20
Q

AEA and 2-AG are

A

lipid soluble and not packaged into vesicles

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21
Q

AEA and 2-AG metabolized by

A

FAAH and MAGL respectively

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22
Q

endocannabinoids generated in pyramidal cells in hippocampus lead to a release of

A

GABA inhibition (increasing firing)

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23
Q

cannabis effects

A

Hypoalgesia (reduced sensitivity to pain)
▸ Increased appetite
▸ Memory impairment

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24
Q

cannabis effects reversed when

A

co-administered with CB1 antagonist like Rimonabant

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25
Q

reinforcing properties potentiated by

A

activating mesolimbic DA system

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26
Q

enhance self-administration of THC

A

opioid antagonists

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27
Q

cannabis tolerance caused by

A

densensitization and downregulation of CB1 receptors

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28
Q

cannabis withdrawal characterized by

A

Irritability, increased anxiety, depressed mood, heightened aggressiveness, decreased appetite (similar to nicotine withdrawal)

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29
Q

cannabis withdrawal mimicked by

A

rimonabant

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30
Q

Indoleamine hallucinogins

A

LSD,psilocybin,DMT

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31
Q

Indoleamines have _ like structure

A

serotonin, agonists of 5-HT2

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32
Q

Highest affinity for

A

2A and 2C subtypes

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33
Q

penethylamines

A

mescaline, amphetamines

34
Q

penethylamines primarily modulate the

A

noradrenergic system

35
Q

less promiscuous than indoleamines at 5-HT2

A

most affinity to 2A and 2C, not other 6

36
Q

Effects of PCP

A

dissociative anaesthetic, detachment from body, cognitive disorganization

37
Q

ketamine is __ PCP

A

less potent and shorter acting than

38
Q

PCP is considered a

A

psychotomimetic

39
Q

PCP/ketamine mechanism of action

A

noncompetitive antagonist of NMDA receptor that binds at unique spot

40
Q

NMDA antagonism in hippocampus and cerebral cortex

A

causes cognitive deficits

41
Q

other noncompetitive NMDA antagonist is

A

DMT

42
Q

ketamine my reduce opioid tolerance and withdrawal by

A

increasing analgesia, slows mechanism of tolerance produced by NMDA

43
Q

reinforcing because increases

A

midbrain DA firing and DA release in PFC

44
Q

Chronic ketamine use causes

A

memory/cognitive deficits
structural abnormalities
cell apoptosis

45
Q

addiction as disease

A

genetic and neural circuit-level mechanisms:
reward vs anti-reward recruitment during drug seeking
positive vs negative reinforcement

46
Q

addiction: routes of administration

A

faster onset, stronger abuse potential (IV and Inhalation)

47
Q

relapse

A

environmental stress, drug priming

48
Q

withdrawal and craving

A

classical conditioning, cues, negative reinforcement

49
Q

___ pathway mediates reinforcing effects

A

mesolimbic dopamine

50
Q

Three theories

A
  1. DA release creates euphoria (false)
  2. Incentive sensitization (drug wanting increases but drug liking stays the same)
  3. DA and reward prediction (VTA neurons predict reward and respond to prediction errors)
51
Q

Koob and Le Moal Model

A

progression from Impulsive (primary motivation is positive reinforcement) to compulsive (primary motivation is negative reinforcement / relief from withdrawal)

52
Q

2 types of neuroadaptations

A
  1. within-system adaptations (down-regulation of reward system)
  2. Between-system adaptations (up-regulation of anti-reward system which increases release of NE, CRF, and amygdala activation)
53
Q

role of PFC

A

healthy: dorsal PFC > ventral PFC (inhibitiory control keeps emotional impulses in check)

drug-addicted:
Ventral PFC > dorsal PFC (emotional, impulsive behavior (short term drug rewards override long term health/behavioral consequences)

54
Q

When experienced cocaine-users take cocaine along with an amino acid mixture that depletes catecholamine levels, these individuals show a reduction in (craving/ hedonic aspects), but no reduction in (craving/hedonic aspects) compared to controls

A

craving, hedonic aspects

55
Q

Neurobiology of anxiety

A

amygdala and BNST

56
Q

amygdala

A

forms associations between fear and environmental stimuli

fear response may become generalized, fear response comes from central amygdala

57
Q

BNST

A

receives input from amygdala, produces state of sustained preparedness

58
Q

chronic stress increases

A

dendritic length, branching, and volume of the BNST

59
Q

stress can also result in a decrease in

A

hippocampal volume, implying memory impairment

60
Q

PFC and Anterior cingulate cortex (ACC) provide

A

top-down control of fear circuitry

61
Q

GAD may be caused in part by reduction in

A

top-down control, resulting in excessive fear signaling

62
Q

3 reasons for heightened anxiety:

A
  1. increased fear signaling in amygdala (generalized fear response)
  2. Decreased top-down control by PFC and ACC
  3. BNST and amygdala hyperactivity in response to unpredictable threat
63
Q

HPA axis in stress/anxiety (4)

A
  1. CRF released in Hypothalamus which binds pituitary, amygdala, hippocampus, and periphery
  2. Pituitary releases ACTH which binds receptors in adrenal cortex
  3. adrenal cortex releases gluocorticoids (cortisol)
  4. elevated cortisol levels trigger negative feedback loop (Inhibit HPA axis)
64
Q

elevated baseline CRF chronically

A

activates HPA axis and results in cell death in hippocampus (reduced volume)

65
Q

prenatal stress model

A

elevated CRF in central amygdala, down-regulated expression of glucocorticoid receptors in hippocampus, reduced negative-feedback

66
Q

NE and epinepherine

A

sympathomimetics, increase LC firing to novel stimuli signaling threat or reward, NE also plays role in formation of emotional memories

67
Q

electrical stimulation of LC or a2 autoreceptor antagonist causes

A

alerting/fear response (anxiogenic)

68
Q

adrenergic beta-blockers (propanolol) impair formation of

A

emotional memories; if given during recall of traumatic memory it will blunt emotional response

69
Q

benzodiazepines (BDZ) can only act on GABA A receptors in the presence of

A

GABA

70
Q

BDZs enhance

A

Cl conductance through GABA (hyperpolarization)

71
Q

SSRIs treat anxiety by increasing action of

A

5-HT (5-HT1A are anxiolytic)

72
Q

Panic disorder patients show reduced

A

BDZ binding sites - increased anxiety is due to reduced GABAergic inhibition, patients need higher doses to reach efficacy

73
Q

depression is characterized by

A

Anhedonia — loss of pleasure/
motivation (impaired reward circuitry)

Hopelessness, desparation,
worthlessness


74
Q

bipolar disorder

A

recurrent episodes of depression, followed by mania

mania- elevated mood, arousal, grandiosity, impulsivity

75
Q

depression and anxiety

A

60% comorbidity of MDD and GAD

76
Q

depression coincides with hyperactive

A

HPA axis, elevated stress hormone levels in blood plasma.

Severe depression/anxiety: elevated CRF and ACTH levels resulting in greater cortisol level

77
Q

concordance rate

A

percentage of twin-pairs where both twins are

affected by disorder

78
Q

mood disorders concordance rate

A

65%

79
Q

bipolar disorder concordance

A

80%

80
Q

genetic factors increase risk, but

A

many other factors involved

BBB 270 Exam 3 Review PPT (1 decks)

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