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neuropharmacology > Neuropharmacology > Flashcards

Neuropharmacology Flashcards

exam

1
Q

alpha1-R

A

stimulatory

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2
Q

alpha2-R

A

inhibitory

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3
Q

GABAA-R

A

inhibitory

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4
Q

NMDA-R and nACh-R

A

excitatory

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5
Q

potency

A

activity of drug in terms of concentration of drug required

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6
Q

thalamus is associated with

A

pain, altertness

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7
Q

Basal ganglia (striatum) associated with

A

movement

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8
Q

hippocampus associated with

A

long term memory and episodic memory, stress response

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9
Q

amygdala associated with

A

emotional memories

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10
Q

Nucleus accumbens (striatum) associated with

A

reward and motivation

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11
Q

Dorsolateral PFC

A

executive function, problem solving

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12
Q

orbitofrontal PFC

A

emotions, impulsivity, decision making

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13
Q

cingulate PFC

A

formation, processing of memories

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14
Q

hypothalamus associated with

A

sleep, appetite

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15
Q

spinal cord associated with

A

pain

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16
Q

inhibitory neurotransmitter

A

GABA

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17
Q

Effect of GABA

A

sedation

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18
Q

Effect of NE

A

mood, arousal, cognition, wakefulness

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19
Q

Effect of 5HT

A

mood, arousal, cognition wakefulness, anxiety, impulsivity

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20
Q

Effect of DA

A

arousal, cognition, reward, movement, impulsivity, addiction

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21
Q

Dopaminergic pathways

A

Mesolimbic, VTA to striatum
Mesocortical, VTA to PFC
Nigrostritial, Substantia nigra to striatum

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22
Q

Mesolimbic dysregulation

A

Addiction , reward pathway

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23
Q

Mesocortical dysfunction

A

negative symptoms in schizophrenia

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24
Q

Nigrostriatial dysfunction

A

movement control, EPS

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25
Q

Effect of histamines

A

wakefulness, executive function

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26
Q

Effect of ACh

A

arousal, sleep, learning, memory

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27
Q

CSTC loop modulates

A

attention, emotion, impulsivity, motor activity

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28
Q

Positive symptoms of schizophrenia

A

characteristics that should not be there eg delusions, hallucination.

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29
Q

Negative symptoms of schizophrenia

A

lack of normal characteristics

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30
Q

symptoms of schizophrenia

A

positive- and negative symptoms, affective symptoms, cognitive function, aggressive symptoms

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31
Q

Hyperactive mesolimbic pathway in schizophrenia according to DA hypothesis

A

positive symptoms

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32
Q

Hypoactive mesocortical pathway in schizophrenia according to DA hypothesis

A

cognitive, affective, negative symptoms

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33
Q

Dopamine hypothesis of schizophrenia

A

disturbed and hyperactive DA transmission

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34
Q

Positive symptoms glutamate hypothesis of schizophrenia

A

Hyperactive mesolimbic DA transmission, due to insufficient GABA feedback to VTA leading to excessive glutamate in VTA, excessive DA in N-Acc

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35
Q

Negative symptoms glutamate hypothesis of schizophrenia

A

Hypoactive mesocoritcal DA transmission

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36
Q

Hypoactiva tuberofudibular pathway

A

Hyperprolactinemia

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37
Q

Glutamate hypothesis

A

NMDA-R dysfunction, compromises GABA feedback causing increased glutaminergic neuron activity. Too much uncoordinated information

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38
Q

Glutamate hypothesis : positive symptoms

A

Hypoactive NMDA-R on GABA neurons leads to increased glutamate in VTA, leading to excessive DA stimulation in mesolimbic DA pathway

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39
Q

Glutamate hypothesis: negative symptoms

A

Hypoactive NMDA-R on GABA neurons leads to increased glutamate in VTA, this leads to excessive stimulation on pyramidal neurons which inhibits mesocortical DA neurons

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40
Q

Nigrostrial pathway (substantia nigto to striatum)

A

EPS

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41
Q

Serotonin hypothesis of schizophrenia

A

increased 5HT in striatum and PFC

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42
Q

Conventional anti psychosis

A

D2 antagonists eg haloperidol.

Dampens positive symptoms (limbic), do not alleviate negative systems.

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43
Q

Side effects of conventional psychotics:

A

Hyperprolactinemia, EPS

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44
Q

Types of EPS:

A

Parkinsonism = parkinson like symptoms like tremor
Akathasia: inability to remain motionless
Dystonia: sustained muscle contractions
Dyskinesia: involuntary movements

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45
Q

Role of 5HT-R

A

5HT1A: depression, anxiety, cognition
5HT2A: sleep, hallucinations, inhibits DA release in nigrostriatal pathway
5HT2C: obesity, mood, cognition

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46
Q

5HT2A-R

A

on GABA neurons inhibit DA transmission in nigrostrial pathway,
stimulate mesolimbic DA transmission by stimulating glutamate neurons

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47
Q

5HT1A-R

A

autoreceptor inhibits 5HT release, less 5HT2A stimulated DA release. Stimulate striatal DA by decreasing 5HT transmission

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48
Q

Atypical antipsychotics

A

reduced EPS tendency, 5HT2A-antagonism, 5HT1A antagonism, D2 rapid dissociation , D2-R partial
only partially normalize negative, cognitive and affective symptoms

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49
Q

side effects atypical antipsychotics

A

Broad antagonism:
alpha1: sedation, dizziness, orthostatic hypotension
H1: weight gain
M1: blurred vision mouth

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50
Q

5HT2C antagonism

A

weight gain, increased cortical DA and NE, mesolimbic DA disinhibition

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51
Q

Symptoms of depression

A

depressed mood, apathy, weight changes, sleep disturbance, guilt, psychomotor, fatigue

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52
Q

reduced positive affect

A

depressed mood, anhedonia, apathy, decreased enthusiasm

= DA and NE deficits

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53
Q

increased negative affect

A

depressed mood, ruminative thoughts, guilt, disgust

=5HT deficits

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54
Q

Monoamine hypothesis

A

depression due to deficient brain monoamine transmission

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55
Q

Activity in different brain regions in depression

A

increased in amygdala, acc, ofc

decreased in striatum

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56
Q

Anhedonia

A

due to reduced response of N.Acc to positive stimuli

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57
Q

Dysregulated HPA axis in depression

A

decreased negative feedback by GR, increase CRH and ACTH and thereby cortisol. Cortisol facilitate mesolimbic DA release which leads negative bias and cognitive deficits

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58
Q

default mode network

A

active during passive rest and mind wandering
self-appraisal, self-evaluation
hyperactive in depression

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59
Q

task positive network

A

active during tasks

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60
Q

SNRI and NRI effect

A

SNRI decrease negative affects

NRI increase positive affects

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61
Q

VMPFC involved in

A

emotional response, self-confidence, self-criticism

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62
Q

DLPFC involved in

A

problem solving, sustained attention, cognitive flexibility

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63
Q

Acc

A

selective attention

64
Q

amygdala

A

associative emotional memory

65
Q

hippocampus

A

conscious long term memory, attribute context to stimuli

66
Q

Neuroinflammatory hypothesis of depression

A

increased production of inflammatory markers

67
Q

Neurogenesis hypothesis

A

antidepressants increase BDNF production which leads to neurogenesis

68
Q

GABA-glutamate hypothesis of depression

A

depressed has Reduced GABA, increased glutamate in CSF

NMDA-R inhibition disinhibit glum release causing more AMPA transmission

69
Q

Reboxetine (NRI)

A

normalize impaired memory of positive words

70
Q

NE regulate 5HT transmission through

A

alpha1 and alpha2 receptors

71
Q

adrenergic autoreceptor

A

alpha2

72
Q

5HT regulate NE through

A

5HT2A (increase DA and NE in PFC) and 5HT2C receptors (reduce DA and NE in PFC)

73
Q

TCAs

A

effective,
side effects due to alpha1 (orthostatic hypotension), M1/M3 (blurred vision, dry mouth constipation) and H1 antagonism (sedation, weight gain), voltage gated Na+ channels (cardiac arrhythmia, seizures)

74
Q

SSRI

A

fluoxetine, setraline, citalopram

may cause apathic recovery by increasing 5HT, the negative affect is improved but positive affects isn’t.

75
Q

SNRI

A

venlaflaxine

improves positive affects better than SSRI

76
Q

NDRI

A

methylphenidate, amphetamine
less sexual side effects
may be nAchR-antagonist

77
Q

NRI

A

reboxetine, amoxetine

78
Q

Other targets

A

melatonin-R agonists (agomelatine), NaSSA (mirtazapine)

79
Q

MAO-I

A

inhibits MAO enzymes
reversible or irreversible
tyramine risk of hypertensive crisis
if given with SERT can cause serotonin syndrome

80
Q

5HT reduce mesolimbic and cortical DA

A

through 5HT2C-R in Acc (GABA, descending glutamate)

81
Q

Delayed action of ADs

A

due to autoreceptor desensitization:

  • chronic NET inhibition can desensitize terminal alpha2-R
  • chronic SERT can desensitize 5HT1A and 5HT1B/D autoreceptors. 5Ht transmission is attenuated by increased 1A stimulation, chronic stimulation leads desensitized 1A-R causing firing to normalize.
82
Q

AMPA and NMDA ratio

A

chronic AD treatment cause decrease in NMDA-R sensitivity, which increase AMPA expression. ADs shifts toward AMPA

83
Q

side effects of SERT inhibition

A

anxiety: 5HT2A/C overactivation
suicidal: changes in 5HT2A transmission
sexual: 5HT1B/C
nausea: 5HT3

84
Q

psilocybin in despression

A

fast acting, long lasting, blast 5HT2A-r stimulation

85
Q

symptoms of anxiety

A

Fear and worry (sleep, concentration, fatigue, arousal, panic attacks)

86
Q

Regulation of fear

A

overreactive connections between amygdala and Acc+OFC

87
Q

Fear expression

A

expressed by motor avoidance (amygdala and PAG), increased cortisol (heart disease, diabetes), increasing respiration rate (PBN via amygdala), increased HR and BP (LC and amygdala)

88
Q

characterization of anxiety disorders

A

excessive and aberrant responding under conditions of threat. Inflated estimates of probability and consequences = judgement bias
can be triggered by traumatic memories hippocampus activating amygdala

89
Q

Fear is amygdala centered

A

emotional response to actual threat/stressor, quick, on-set, brief
panic, phobia

90
Q

anxiety is CSTC centered

A

sustained emotional response to unpredictable threat

anxious misery, obsessions

91
Q

Cause of fear and worry

A

amygdala hyperactivity causing glutamate release

BDZ, alpha2delta, SERT, 5HT1A-R reduce this

92
Q

GAD (anxiety based)

A

generalized and persistent anxiety - not restricted to particular circumstances.
symptoms are nervousness, sweating, trembling
intolerance of uncertainty
dysregulated HPA axis, elevated cortisol, low GABAA-R
treated with: SSRI, SNRI alpha2delta ligands, 5HT1A-R partial agonist

93
Q

PD (fear based)

A

recurrent panic attacks not restricted to particular circumstances
chest pain, choking, dizziness
No HPA dysregulation
SSRI, SNRI, alpha2delta ligands
avoidance maintained by cognitive appraisal

94
Q

Phobia (fear based)

A

anxiety evoked in well-defined situations
focused on individual symptoms
SSRI, SNRI, alpha2delta ligands
beta-blockers may dampen blushing, tremor, nausea

95
Q

PTSD (anxiety based)

A

reexperiencing and avoiding traumatic memories
traumatic stressor is criteria
due to decreased alpha2R sensitivity leading to increased cortical NE
sensitized HPA -> low cortisol
SNRI, SSRI, alpha-delta ligands, alpha1 antagonists prevents nightmares

96
Q

OCD

A

recurrent obsessive thoughts, compulsive rituals, if resisted anxiety gets worse

97
Q

buspirone is partial 5HT1A agonist

A

-

98
Q

NE hyperactivation in anxiety

A

= anxiety, panic, tremor,

treat with alpha1 or beta blockers

99
Q

Fear extinction

A

progressive reduction of response to stimuli as VMPFC learns new context for feared stimuli. Produces GABA inhibition by activating glutamate neurons

100
Q

fear conditioning

A

stressfull stimuli is relayed to amygdala and integrated with input from VMPFC and hippocampus. Amygdala may remember stimuli and increase efficiently of glutamate neurontransmission making future response more efficiently triggered.

101
Q

MDMA in anxiety

A

reduce sense of fear by increasing 5HT2A-R, Ne, DA, alpha2 activation

102
Q

Rem sleep is characterized by

A

motor atonia = due to sleep specific ACh activated inhibitory circuit

103
Q

brain region allowing sleep

A

hypothalamus filtering out sensory transmission

104
Q

wakepromoting neurotransmitters

A

5HT, NE, Ach, histamine

105
Q

sleep promoting neurotransmitters

A

MCH, GABA, ACh, adenosine

106
Q

high firing neurotransmitters in REM

A

ACh

107
Q

high firing neurotransmitters in awake

A

ACh, 5HT, NE, H

108
Q

Adenosine hypothesis

A

increases sleep. Accumulating extra cellular concentration during wakefulness. The increased concentration inhibits waker,oyinh cells, when this activity is sufficiently decreased sleep is induced. Concentration decrease during sleep.

109
Q

Orexin neurons

A 
located in lateral hypothalamus. 
fire in awake, silent in asleep. 
induce behavioral arousal
excites Ach neurons in wakefullness, 5HT, H, Ne all involved in wakefullness 
= Arousal
110
Q

MCH (melanin concentrating hormone)

A

in lateral hypothalamus

increase REM duration, release GABA

111
Q

wake promoting regions

A

LC, TMN, raphe

112
Q

melatonin

A

SCN passes information onto pineal gland which synthesize and secrete melatonin, inhibited by light exposure
increases sleepiness, master clock for timing

113
Q

insomnia

A

disruption of thalamic filters i CSTC loops
-> local thalamic GABA transmission deficient at night = massive sensory input
OR
stress activating HPA axis, increasing cortisol blocks sleep

114
Q

consequences of sleep deprivation

A

increased BP, mood changes, elevated metabolic rate hyperalgesia

115
Q

Sleep wake switch

A

in hypothalamus.
VLPO is sleep switch mediated by GABA
TMN is wake switch mediated by Histamine

116
Q

Drugs for insomnia

A

GABAA-PAMs (BDZ, barbiturates, z-drugs), histamine drugs (H1 antagonism), melatonin (M1/M2 agonism)

117
Q

EDS

A

problem with sleep/wake switch

treated with wakefulness drugs like orexin agonists

118
Q

Drugs causing sedation

A

histamine, anticholinergic, alpha adrenergic, 5Ht enhancers, melatonin-R agonists

119
Q

Restless leg syndrome,e

A

cause of insomnia
urge to move legs, relieving pain, worsening at rest
ion deficiency
alpga2 agonistst, Da agonists, opioids, BDZ

120
Q

sleep disturbance indicators

A

high NE and CRH

121
Q

REM sleep behavior disorder

A

vigorous and injurious behavior in REM sleep,

122
Q

Narcolepsy treatment

A

treated with GHB, midnafinil, amphetamine,

123
Q

function of sleep

A

maintain healthy immune system (comprises immune system), metabolism (risk of metabolic syndrome), healthy cognition.

124
Q

function of sleep

A

maintain healthy immune system (comprises immune system), metabolism (risk of metabolic syndrome), healthy cognition.

125
Q

symptoms of ADHD

A

hyperactivity, impulsivity, sustained attention, selective attentive

126
Q

selective attention in ADHD due to

A

unability to activate ACC this recruiting other regions (dysfunctional CSTC-loop)

127
Q

Motor activity in ADHD due to

A

regulation by PFMC

dysfunctional CSTC-loop

128
Q

Sustained attention in ADHD due to

A

regulation by DLPFC

dysfunctional CSTC-loop

129
Q

Impulsivity in ADHD due to

A

regulation by OFC

dysfunctional CSTC-loop

130
Q

Insufficient NE/DA in ADHD

A

distracted, impulsive, poor judgement, impaired working memory,

131
Q

Excessive NE/DA in ADHD

A

stressed, hyperactive, distractible, inattentive

132
Q

Fine tuning signal-to-noise ratio in ADHD

A

hypofrontality in PFC for executive functioning.
NE increase sensitivity for relevant stimuli, DA decrease sensitivity for irrelevant stimuli
alpha2 and D1 receptors on dendritic spines gate incoming signals.
If HCN channel is open, signal leaks and is lost.
NE keeps channel closed, DA opens channel.

133
Q

default mode network in ADHD

A

interrups task positive network during attention tasks

134
Q

treatment of ADHD

A

methylphenidate, ampetamine, amoxetine, guanfacine, stimulants (normalize mesolimbic DA, reduce amygdala)

135
Q

Reuptake transporters in PFC

A

low DAT, high NET

136
Q

Reuptake transporters in NAcc

A

low NET, high DAT

137
Q

Gate control theory

A

Abeta-fibers can disrupt sensation of pain, by exciting neurons that can inhibit pain carrying neurons by releasing GABA

138
Q

Neuropathic pain

A

pain caused by lesion or disease of somatosensory nervous system

139
Q

Abeta fibers

A

non-noxious, mechanical stimuli (myelinated)

140
Q

Adelta fibers

A

noxious, chemical stimuli (myelinated)

141
Q

C fibers

A

noxious, heat and chemical stimuli (unmyelinated)

142
Q

Delaying discount in ADHD

A

decay of subjective experience of reward value, if reward delivery is delayed
- delays faster in impulsive
- challenges ability to tolerate delayed gratification.
lack of DA response to stimuli can cause distress and delayed gratification.
(less striatal response to reward anticipation in DA, more to reward delivery)

143
Q

segmentral central sensitization

A

can increase pain as chronic firing in dorsal horn leads to exaggerated or prolonged response to inputs

144
Q

suprasegmentral central sensitization

A

from peripheral injury

  • thalamus or cortex amplifies pain
  • pain can occur without peripheral input
145
Q

Desccending NE and 5HT

A

can inhibit pain

146
Q

treatment of neuropathic pain

A

TCA, SSRI, SNRI, anticonvulsants

147
Q

inherent reward

A

intrinsic

148
Q

not inherent reward

A

extrinsic

149
Q

Intensifying hedonic experiences

A

DA release in NAcc

can be stimulated by coke, my-opioid R

150
Q

repeated opioid use

A

cause down regulation of my-opioid-R leading my tolerance and dependence

151
Q

BDZ in addiction

A

disinhibit reward circuit, chronic use down regulate GABAA-R = tolerance and dependence

152
Q

Alcohol

A

PAM at GABAA-R, chronic intake down regulate expression extrasynaptically -> leading to decreased excitability of neurons, chronic reduce baseline GABA transmission and increase glutamate,
stimulate my-opioid-R, Cb1 activation

153
Q

Gateway hypothesis

A

alcohol, nicotine, cannabis are gateway drugs increasing risk of moving on to harder drugs

154
Q

diagnostic criteria for addiction

A

impaired control, social impairment, risky use of substance, pharmacological criteria

155
Q

Tolerance

A

reduction in drug effect, requiring increased dose to maintain effective dose

156
Q

Dependence

A

response to a drug whereby removal gives unpleasant symptoms

157
Q

Addiction

A

drug taker feels compelled to use drug and suffers from anxiety when separated

neuropharmacology (1 decks)

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