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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
reinforcing properties potentiated by
activating mesolimbic DA system
26
enhance self-administration of THC
opioid antagonists
27
cannabis tolerance caused by
densensitization and downregulation of CB1 receptors
28
cannabis withdrawal characterized by
Irritability, increased anxiety, depressed mood, heightened aggressiveness, decreased appetite (similar to nicotine withdrawal)
29
cannabis withdrawal mimicked by
rimonabant
30
Indoleamine hallucinogins
LSD,psilocybin,DMT
31
Indoleamines have _ like structure
serotonin, agonists of 5-HT2
32
Highest affinity for
2A and 2C subtypes
33
penethylamines
mescaline, amphetamines
34
penethylamines primarily modulate the
noradrenergic system
35
less promiscuous than indoleamines at 5-HT2
most affinity to 2A and 2C, not other 6
36
Effects of PCP
dissociative anaesthetic, detachment from body, cognitive disorganization
37
ketamine is __ PCP
less potent and shorter acting than
38
PCP is considered a
psychotomimetic
39
PCP/ketamine mechanism of action
noncompetitive antagonist of NMDA receptor that binds at unique spot
40
NMDA antagonism in hippocampus and cerebral cortex
causes cognitive deficits
41
other noncompetitive NMDA antagonist is
DMT
42
ketamine my reduce opioid tolerance and withdrawal by
increasing analgesia, slows mechanism of tolerance produced by NMDA
43
reinforcing because increases
midbrain DA firing and DA release in PFC
44
Chronic ketamine use causes
memory/cognitive deficits structural abnormalities cell apoptosis
45
addiction as disease
genetic and neural circuit-level mechanisms: reward vs anti-reward recruitment during drug seeking positive vs negative reinforcement
46
addiction: routes of administration
faster onset, stronger abuse potential (IV and Inhalation)
47
relapse
environmental stress, drug priming
48
withdrawal and craving
classical conditioning, cues, negative reinforcement
49
___ pathway mediates reinforcing effects
mesolimbic dopamine
50
Three theories
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
Koob and Le Moal Model
progression from Impulsive (primary motivation is positive reinforcement) to compulsive (primary motivation is negative reinforcement / relief from withdrawal)
52
2 types of neuroadaptations
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
role of PFC
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
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
craving, hedonic aspects
55
Neurobiology of anxiety
amygdala and BNST
56
amygdala
forms associations between fear and environmental stimuli fear response may become generalized, fear response comes from central amygdala
57
BNST
receives input from amygdala, produces state of sustained preparedness
58
chronic stress increases
dendritic length, branching, and volume of the BNST
59
stress can also result in a decrease in
hippocampal volume, implying memory impairment
60
PFC and Anterior cingulate cortex (ACC) provide
top-down control of fear circuitry
61
GAD may be caused in part by reduction in
top-down control, resulting in excessive fear signaling
62
3 reasons for heightened anxiety:
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
HPA axis in stress/anxiety (4)
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
elevated baseline CRF chronically
activates HPA axis and results in cell death in hippocampus (reduced volume)
65
prenatal stress model
elevated CRF in central amygdala, down-regulated expression of glucocorticoid receptors in hippocampus, reduced negative-feedback
66
NE and epinepherine
sympathomimetics, increase LC firing to novel stimuli signaling threat or reward, NE also plays role in formation of emotional memories
67
electrical stimulation of LC or a2 autoreceptor antagonist causes
alerting/fear response (anxiogenic)
68
adrenergic beta-blockers (propanolol) impair formation of
emotional memories; if given during recall of traumatic memory it will blunt emotional response
69
benzodiazepines (BDZ) can only act on GABA A receptors in the presence of
GABA
70
BDZs enhance
Cl conductance through GABA (hyperpolarization)
71
SSRIs treat anxiety by increasing action of
5-HT (5-HT1A are anxiolytic)
72
Panic disorder patients show reduced
BDZ binding sites - increased anxiety is due to reduced GABAergic inhibition, patients need higher doses to reach efficacy
73
depression is characterized by
Anhedonia — loss of pleasure/ motivation (impaired reward circuitry) Hopelessness, desparation, worthlessness

74
bipolar disorder
recurrent episodes of depression, followed by mania | mania- elevated mood, arousal, grandiosity, impulsivity
75
depression and anxiety
60% comorbidity of MDD and GAD
76
depression coincides with hyperactive
HPA axis, elevated stress hormone levels in blood plasma. | Severe depression/anxiety: elevated CRF and ACTH levels resulting in greater cortisol level
77
concordance rate
percentage of twin-pairs where both twins are | affected by disorder
78
mood disorders concordance rate
65%
79
bipolar disorder concordance
80%
80
genetic factors increase risk, but
many other factors involved

BBB 270 Exam 3 Review PPT (1 decks)

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