Exam 3 Flashcards
(113 cards)
1
Q
serotonin is synthesized from what
A
tryptophan
2
Q
two steps to serotonin synthesis
A
catalyzed by TPH and AADC
3
Q
TPH2
A
in serotonergic neurons
4
Q
how is serotonin synthesis regulated
A
enzymatic activity and precursor activity
5
Q
why does tryptophan compete with amino acids
A
to cross the blood brain barrier and increase serotonin
6
Q
what diet increases ratio of tryptophan
A
low protein high carbohydrate
7
Q
what does elevating tryptophan do
A
enhance cognitive functions (memory, attention), elevate mood, improve sleep
8
Q
tryptophan loading
A
administration of pure tryptophan
9
Q
if you inhibit TPH you get
A
less serotonin
10
Q
reducing serotonin via ATD method does what
A
impairs memory consolidation of verbal information but has no influence on working memory and attention
11
Q
serotonin is transported into synaptic vesicles by
A
VMAT2
12
Q
reserpine does what
A
depletes serotonin (broken down when not in vesicles)
13
Q
terminal autoreceptors do what to serotonin
A
directly inhibit release
14
Q
somato-dendritic autoreceptros do what to serotonin
A
inhibit release by slowing rate of nerve firing
15
Q
what reuptakes serotonin
A
SERT
16
Q
antidepressant drugs
A
SSRI’s
17
Q
how do SSRIs work
A
by blocking the serotonin transporter
18
Q
where are serotonergic neurons found
A
along the midline of the brainstem (raphe nuclei)
19
Q
what are the roles of dorsal raphe nucleus (DRN) and median raphe nucleus (MRN)
A
give rise to most of the serotonergic fibers in forebrain
20
Q
when awake, how do serotonin cells fire
A
a regular rate (tonic firing)
21
Q
how do serotonin cells fire when in slow wave sleep
A
irregularly
22
Q
slow tonic firing of DRN neurons promotes what
A
non REM sleep
23
Q
burst firing of DRN neurons promotes what
A
wakefulness
24
Q
where is serotonin 1a receptor concentrated
A
in hippocampus, septal area, and DRN
25
what does the serotonin 1A receptor do
inhibit adenylyl cyclase to decrease cAMP, increase opening of K+ channels and membrane hyperpolarization
26
what kind of receptor is serotonin 1A
autoreceptor and postsynaptic
27
where are serotonin 2A receptors located
cortex
28
what do serotonin 2a receptors do
increase Ca2+ levels in postsynaptic cell and activate protein kinase C
29
what kind of receptor is serotonin receptor 2A
activating
30
most serotonergic neurons in the CNS are located
raphe nuclei
31
serotonin has a key role in regulation of
anxiety through postsynaptic serotonin 1A receptors
32
serotonin deficiency hypothesis
low CNS serotonergic activity is associated with hyper aggressiveness
33
what is a behavior/function influenced by serotonin
anxiety, appetite, and sleep
34
what does MDMA do
stimulates release of serotonin from nerve terminals and inhibits reuptake
35
effects of MDMA
heightened arousal, euphoria, enhanced perceptual awareness, prosocial effects
36
high MDMA doses result in
serotonin depletion (in animals)
37
designer drugs
synthetic cathinone and amphetamine variants
38
synthetic cathinones
are substrates for dopamine, norepinphrine, and serotonin transporters, and cause acute release of dopamine, serotonin, and norepinephrine
39
what kind of drugs are opioids
narcotic analgesics (reduce pain without producing uncosciousness)
40
psychoactive ingredients in opiates
morphine and codeine
41
partial agonists
less analgesic effect, reduced risk of dependence
42
antagonist
can prevent or reverse effects of opioids (treatment for overdose)
43
which reaches the brain faster: heroin or morphine
heroin
44
adverse affects of opoids
restlessness, anxiety, nausea/vomiting
45
higher doses of opiods
abnormal state of elation or euphoria
46
low to moderate dose of opioid
pain relief, constricted pupils, drowsiness, inability to concentrate, dreamy sleep
47
respiratory failure is the ultimate cause of death in overdose because
morphine acts on the brainstem's respiratory center
48
how can naloxone's blocking effects be overcome
by increasing concentrations of morphine, showing competition for the receptor
49
types of opioid receptors
mu, delta, and kappa
50
mu receptors
have a high affinity for morphine, wide distribution in brain and spinal cord
51
delta receptors
found in forebrain, modulate olfaction, motor integration, reinforcement, and cognitive function
52
kappa receptors
found in striatum and amygdala, hypothalamus and pituitary, participate in regulation of pain perception, gut motility, and dysphoria
53
all opioid receptors are coupled to
G proteins (metabotropic, all inhibitory)
54
postsynaptic inhibition
opens potassium channels, hyperpolarization
55
axoaxonic inhibition
closes calcium channels, decreases amount of transmitter released
56
presynaptic autoreceptors
reduce release of a co-localized transmitter
57
mu and delta receptor join to form
a heterodimer
58
opioid ligands are
peptides
59
mu receptor binds to
endomorphins and endorphins
60
delta receptor binds to
enkephalin
61
kappa receptor binds to
dynorphins
62
first (early) pain
immediate, sensory component, goes from spinal cord to thalamus
63
second (late) pain
emotional component, goes to anterior cingulate cortex
64
opioids reduce transmission of pain signals at the spinal cord in two ways
inhibitory spinal interneurons: release endorphins that inhibit activation of spinal projection neurons
descending modulatory pathways: inhibit projection neuron or excitatory interneuron, or excite inhibitory opioid neuron
65
opioid drugs inhibit
inhibitory GABA cells, increasing mesolimbic cell firing and dopamine release in NAcc
66
cross tolerance
related drugs also show reduced effectiveness
67
physical dependence
lack of drug causes withdrawal
68
cross dependence
administering any other opioid drug will stop or reduce withdrawal
69
acute effects of opioids are the opposite of
withdrawal symptoms
70
methadone
reduces symptoms to a comfortable level, reduces euphoric effect of heroin
71
clonidine
acts on noradrenergic autoreceptors to reduce norepinephrine activity in locus coeruleus
72
buprenorphine
opioid partial agonist used in the same way as methadone
73
medication assisted treatment
a combination of detoxification, pharmacological support, and group/individual counseling
74
glutamate
ionized form of glutamic acid formed from glutamine (an excitatory amino acid neurotransmitter)
75
vesicular glutamate
transporters move glutamate into synaptic vesicles: VGLUT1, 2, and 3
76
glutamate uptake
5 different excitatory amino acid transporters (EAATs)
77
astrocytes
express EAAT2 and may account for about 90% of total glutamate uptake
78
astrocyte transporters
convert the glutamate uptaken to glutamine using glutamine synthetase
79
ionotropic glutamate receptors
depolarize the membrane of the postsynaptic cell (excitatory)
80
AMPA receptor
fast excitatory responses to glutamate
81
Kainate receptor
selective agonist kainic acid
82
NMDA receptor
allows both Na and Ca to pass, agonist NMDA
83
unique characteristics of NMDA receptors
simultaneous binding of glutamate and a co-agonist
binding site for Mg in the ion channel
channel only opens if both co-agonist binding and depolarization of cell membrane occur
84
metabotropic glutamate receptors
group 1: postsynaptic, activate second messenger system, excitatory
group 2 and 3: presynaptic, reduce transmitter release, inhibit cAMP formation, autoreceptors
85
long term potentiation
release of glutamate coupled with strong activation of NMDA receptors can lead to strengthening of that synapse
86
excitotoxicity hypothesis
excessive exposure to glutamate causes prolonged depolarization of receptive neurons, leading to damage or death
87
GABA
major inhibitory amino acid transporter
88
GABA is synthesized from
glutamic acid decarboxylase (GAD)
89
moves GABA into vesicles
VGAT
90
GABA is metabolized to succinate by
GABA-T
91
GABA a receptor
ionotropic, causes hyperpolarization and inhibition of postsynaptic cell, consists of 5 subunits
92
GABA a receptors are sensitive to
CNS depressant drugs
93
GABA b receptor
metabotropic, postsynaptic, inhibits neuronal firing and adenylyl cyclase
94
Presynaptic GABA b receptors inhibit
transmitter release and adenylyl cyclase
95
diverse group of compounds that depress the CNS and behavior
alcohol, barbiturates, non-barbiturate hypnotics, anxiolytics
96
the calming of mental excitement or abatement of physiological function
sedation
97
to produce sleep
hypnosis
98
behavioral effects of alcohol are described through
blood alcohol concentration (BAC)
99
alcohol is oxidized by
alcohol dehydrogenase and aldehyde dehydrogenase (ALDH)
100
when alcohol is consumed on a regular basis, these liver enzymes increase in number, increasing the rate of metabolism of alcohol/other drugs
induction
101
in a single exposure, effects are greater while blood level is rising and smaller while blood level is falling
acute tolerance
102
increase in P450 liver microsomal enzymes that metabolize alcohol
metabolic tolerance
103
neurons adapt to continued presence of alcohol by making compensatory changes in cell function
pharmacodynamic tolerance
104
practicing behaviors while under the influence of alcohol allows adjustment and compensation
behavioral tolerance
105
intensity and duration of withdrawal is dependent on amount and duration of drug taking
physical dependence
106
permanent damage to thalamic nuclei and brain regions involved in memory subsequent to vitamin B1 deficiency
korsakoff syndrome
107
symptoms of fetal alcohol syndrome
intellectual disability, developmental delays, low birthweight, neurological problems, head/facial malformation
108
why are animal models vital for alcohol research
kept in controlled environment, eliminates poor nutrition, psychiatric disorders, other drug use, genetic engineering can be used
109
cell membrane lipids become more fluid, changes relationship with membrane proteins
nonspecific action
110
influences ligand gated channels and alters second messenger systems
specific actions
111
acute alcohol inhibits
glutamate transmission and glutamate release
112
acute alcohol increases
GABA effects at GABA a receptor
113
