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Neuro unit 1 > CNS neuropharmacology > Flashcards

CNS neuropharmacology Flashcards

1
Q

Behaviors linked to pre frontal cortex

A

executive function and attention, motor, pain, negative symptoms (guilt, suicidality)

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2
Q

Behaviors linked to basal forebrain

A

memory

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3
Q

Behaviors linked to nucleus accumbens

A

delusions, hallucinations, reward

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4
Q

Behaviors linked to striatum

A

motor

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5
Q

Behaviors linked to thalamus

A

pain, sensory relay

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6
Q

Behaviors linked to hypothalamus

A

sleep

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7
Q

Behaviors linked to cerebellum

A

motor

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8
Q

Behaviors linked to spinal cord

A

pain

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9
Q

Behaviors linked to hippocampus

A

memory

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10
Q

Behaviors linked to amygdala

A

fear, anxiety panic

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11
Q

List the precursors and key enzymes for the synthesis of acetylcholine

A

Acetyl-CoA + Choline > ACH + CoA (catalyzed by choline acetyl transferase)

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12
Q

Describe the inactivation mechanisms for acetylcholine

A

acetylcholinesterase

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13
Q

Which receptors does Ach bind to and what are its actions

A

Muscarinic receptors: (M1-M3: Gq stimulate PLC activity) (M2-M4: Gi/o inhibit adenylyl cyclase activity). Nicotinic receptors: Nn opens receptor-gated cation channel [ionotropic]

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14
Q

CNS location of ACH

A

Produced in cell bodies in brain stem and basal forebrain of neurons that widely project to cerebral cortex and hippocampus

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15
Q

Name compounds that affect ACH release, activation and degredation

A

Botulism decreases release, black widow spider venom increases release, Nicotine (nicotinic agonist), Benztropine (muscarinic antagonist) and diphenhydramine (muscarinic antagonist) all work at the receptor. Donepezil is an ACHE inhibitor

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16
Q

List the precursors and key enzymes for the synthesis of biogenic amines

A

Catecholamines: Tyrosine > tyrosine hydroxylase converts to L-Dopa (rate limiting) > dopamine > Norepinephrine > epinephrine. Indoleamine (5-HT): Tryptophan > tryptophan hydroxylase converts to 5-OH-tryptophan (rate limiting) > 5-HT > 5-HIAA

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17
Q

How are monoamines stored

A

Transmitter is taken-up into storage vesicle via the vesicular monoamine transporter (VMAT) where it is packaged for release and protected from
degradation by intraneuronal monoamine oxidase (MAO).Transmitter is taken-up into storage vesicle via the vesicular monoamine transporter (VMAT) where it is packaged for release and protected from
degradation by intraneuronal monoamine oxidase (MAO).Transmitter is taken-up into storage vesicle via the vesicular monoamine transporter (VMAT) where it is packaged for release and protected from
degradation by intraneuronal monoamine oxidase (MAO).

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18
Q

Monoamine termination of action

A

reuptake by presynaptic membrane: dopamine transporter (DAT), norepinephrine transporter (NET), serotonin transporter (SERT)

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19
Q

List receptors/second messengers for norepinephrine

A

α1 adrenergic: Gq stimulation of phospholipase C activity. α2 adrenergic: Gi/o inhibition of adenylyl cyclase activity, K+ channel opening. β1 adrenergic: Gs stimulation of adenylyl cyclase activity. β2 adrenergic: Gs stimulation of adenylyl cyclase activity

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20
Q

List receptors/second messengers for dopamine

A

D1 dopamine receptor: Gs stimulation of adenylyl cyclase activity. D2 dopamine receptor: Gi/o inhibition of adenylyl cyclase activity

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21
Q

List receptors/second messengers for serotonin

A

5HT1A, 1B, 1D: Gi/o inhibition of adenylyl cyclase activity and K+ channel opening. 5HT2A, 2B, 2C: Gq stimulation of phospholipase C activity - closing of Ca++ channel. 5HT3: Ligand-gated cation channel - excitatory [ionotropic]. 5HT4: Gs stimulation of adenylyl cyclase activity

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22
Q

CNS location for dopamine, norepinephrine and serotonin

A

 Dopamine: Substantia nigra > neostriatum pathway (nigrostriatal), ventral tegmental area >
limbic cortex (mesolimbic), ventral tegmental area > frontal cortex pathway (mesocortical),
hypothalamus > pituitary (tuberoinfindibular pathway).  Norepinephrine: Cell bodies in pons and brain stem (locus ceruleus) projecting to all levels of brain  Serotonin: Cell bodies in raphe regions of pons / upper brain stem that project to all levels of brain.  Dopamine: Substantia nigra > neostriatum pathway (nigrostriatal), ventral tegmental area >
limbic cortex (mesolimbic), ventral tegmental area > frontal cortex pathway (mesocortical),
hypothalamus > pituitary (tuberoinfindibular pathway).  Norepinephrine: Cell bodies in pons and brain stem (locus ceruleus) projecting to all levels of brain  Serotonin: Cell bodies in raphe regions of pons / upper brain stem that project to all levels of brain.  Dopamine: Substantia nigra > neostriatum pathway (nigrostriatal), ventral tegmental area >
limbic cortex (mesolimbic), ventral tegmental area > frontal cortex pathway (mesocortical),
hypothalamus > pituitary (tuberoinfindibular pathway).  Norepinephrine: Cell bodies in pons and brain stem (locus ceruleus) projecting to all levels of brain  Serotonin: Cell bodies in raphe regions of pons / upper brain stem that project to all levels of brain.

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23
Q

Function of dopamine, norepinephrine and seretonin

A

dopamine: initiate voluntary movement, rewar related behaviors, working memory, control of attention. Norepi: arousal, attention, vigilance, sleep wake cycle, fear, anxiety. Serotonin: sleep, arousal, attention, sensory info processing, emotion/mood, pain, eating/drinking

24
Q

List drugs that work on norepi action via synthesis, storage, release or termination

A

a-methyl-p-tyrosine decreases synthsis. Reserpine inhibits storage (VMAT). Amphetamine increases release (NET). Cocaine-Bupropion-Venlafaxine inhibit termination (NET) and Phenelzine inhibits termination (MAOa)

25
Q

Where do pseudoephedrine, clonidine, mirtazapine and propranolol act

A

α1 > Pseudoephedrine [indirect ag]
α2 > Clonidine [ag] / Mirtazapine [antag]
β 1-2 > Propranolol
α1 > Pseudoephedrine [indirect ag]
α2 > Clonidine [ag] / Mirtazapine [antag]
β 1-2 > Propranolol
α1 > Pseudoephedrine [indirect ag]
α2 > Clonidine [ag] / Mirtazapine [antag]
β 1-2 > Propranolol

26
Q

Synthesis of GABA

A

glutamate > glutamic acid decarboxylase converts to GABA (gamma-aminobutyric acid)

27
Q

Termination of GABA

A

reuptake into presynaptic nerve and glial cells by GABA transporter

28
Q

List 3 drugs that work on GABA at the synapse and their functions

A

Benzodiazepines: Bind to GABAa (on post-synaptic membrane) receptor to facilitate GABA inhibitory action. Tiagabine: Inhibits reuptake of GABA by

transporter. Vigabatrin: Inhibits degradation by GABA-T (GABA transaminase)Benzodiazepines: Bind to GABAa (on post-synaptic membrane) receptor to facilitate GABA inhibitory action. Tiagabine: Inhibits reuptake of GABA by
transporter. Vigabatrin: Inhibits degradation by GABA-T (GABA transaminase)Benzodiazepines: Bind to GABAa (on post-synaptic membrane) receptor to facilitate GABA inhibitory action. Tiagabine: Inhibits reuptake of GABA by
transporter. Vigabatrin: Inhibits degradation by GABA-T (GABA transaminase)

29
Q

GABA receptors and second messengers

A

GABAa: Opens ligand-gated Cl- channel > decreases neuronal excitability (IPSPs) [ionotropic]. GABAB : Gi/o > inhibit adenylyl cyclase, decrease Ca++ conductance, open K+ channel

30
Q

GABA location/ function

A

brain and spinal cord - major inhibitory neurotransmitter of CNS

31
Q

Glutamate synthesis

A

Glutamine > converted to glutamate by glutaminase

32
Q

Glutamate termination

A

reuptake by neuron via neuronal glutamate transporter, or uptake by glial cell transporter where it is converted to glutamine by glutamine synthetase, then taken up by neuron

33
Q

Glutamate receptors and second messengers

A

NMDA: Increase Ca++ influx. AMPA: Increase Na+ and Ca++ influx. Kainate: Increase Na+ influx. R1-R5 (Group I): Gq > stimulation of phospholipase C activity. R2-R3 (Group II): Gi/o > inhibition of adenylyl cyclase activity-inhibit VSCC-activate K+

channels. R4-R6-R7-R8 (Group III): Gi/o > inhibition of adenylyl cyclase activity-inhibit VSCCNMDA: Increase Ca++ influx. AMPA: Increase Na+ and Ca++ influx. Kainate: Increase Na+ influx. R1-R5 (Group I): Gq > stimulation of phospholipase C activity. R2-R3 (Group II): Gi/o > inhibition of adenylyl cyclase activity-inhibit VSCC-activate K+
channels. R4-R6-R7-R8 (Group III): Gi/o > inhibition of adenylyl cyclase activity-inhibit VSCC

34
Q

Alzheimer’s disease pathology and treatment related to cholinergic pathway

A

Pathology: decreased muscarinic-cholinergic function
Treatment: cholinesterase inhibitors: DonepezilPathology: decreased muscarinic-cholinergic function
Treatment: cholinesterase inhibitors: Donepezil

35
Q

Parkinson’s disease pathology and treatment related to cholinergic pathway

A

Pathology: muscarinic-cholinergic overactivity
Treatment: muscarinic antagonist: Benztropine Pathology: muscarinic-cholinergic overactivity
Treatment: muscarinic antagonist: Benztropine

36
Q

Psychoses pathology and treatment related to cholinergic pathway

A

Pathology: [??] decreased nicotinic-cholinergic function. Treatment: nicotinic agonist: Nicotine

37
Q

Depression pathology and treatment related to adrenergic pathway

A

Pathology: decreased NE activity in cortical areas
Treatment: increase NE activity (acutely) by
1. decrease termination (NET)( Venlafaxine-Amitriptyline), 2. decrease degradation > increase storage - release (MAOA)(Phenelzine) or 3. increase release >α2 antagonist ( Mirtazapine)Pathology: decreased NE activity in cortical areas
Treatment: increase NE activity (acutely) by
1. decrease termination (NET)( Venlafaxine-Amitriptyline), 2. decrease degradation > increase storage - release (MAOA)(Phenelzine) or 3. increase release >α2 antagonist ( Mirtazapine)

38
Q

Pain pathology and treatment related to adrenergic pathway

A

Pathology: abnormal neurotransmission in pain pathway (NE). Treatment: decrease termination (NET): Venlafaxine-Amitriptyline

39
Q

Anxiety pathology and treatment related to adrenergic pathway

A

Pathology: excessive NE neuronal activity. Treatment: β1-β2 antagonist: Propranolol
Pathology: excessive NE neuronal activity. Treatment: β1-β2 antagonist: Propranolol

40
Q

Describe roles of L-dopa, amphetamine, Ropinirole, aripiprazole, haloperidol, cocaine and bupropion on the dopaminergic synapse

A

L-Dopa increases synthesis, amphetamine increases release, Ropinirole is a D2 agonist, Aripiprazole is dopamine partial agonist, haloperidol is D2 antagonist, cocaine inhibits reuptake and bupropion inhibits reuptake (NDRI)

41
Q

Parkinson’s disease pathology and treatment related to dopaminergic pathway

A

Pathology: decreased DA activity in nigrostriatal pathway. Treatment: increase striatal dopamine levels by 1. increase synthesis: L-dopa. 2. increase receptor activation: Ropinirole. 3. decrease degradation, increase storage - release: Carbidopa (DDC) -Selegiline (MAOB) - Entacapone (COMT)

42
Q

Psychoses pathology and treatment related to dopaminergic pathway

A

Pathology: increased DA activity in mesolimbic pathway. Treatment: dopamine D2 antagonist: Haloperidol

43
Q

Describe the roles of Fenfluramine, Buspirone, sumatriptan, clozapine, ondansetron, propranolol, fluoxetine, venlafaxine and clomipramine on the serotoninergic system

A

Fenfluramine increases release, Buspirone is a 5HT1A Partial Agonist, Sumatriptan is a 5HT1D Agonist , Clozapine is a 5HT2A Antagonist, Ondansetron is a 5HT3 Antagonist, Propranolol is a β1-β2 Antagonist, Fluoxetine is a SSRI inhibitor, Venlafaxine is a SNRI inhibitor, Clomapramine is a TCAD reuptake inhibitor

44
Q

Depression pathology and treatment related to seretonin pathway

A

Pathology: decreased 5HT activity in cortical areas
Treatment: increase 5HT activity (acutely) by 1. decrease termination (SERT): Fluoxetine-Venlafaxine. 2. decrease degradation: increase storage - release: (MAOA): PhenelzinePathology: decreased 5HT activity in cortical areas
Treatment: increase 5HT activity (acutely) by 1. decrease termination (SERT): Fluoxetine-Venlafaxine. 2. decrease degradation: increase storage - release: (MAOA): Phenelzine

45
Q

Pain pathology and treatment related to seretonin pathway

A

Pathology: abnormal neurotransmission in pain pathway. Treatment: decrease termination (SERT): Venlafaxine-Duloxetine

46
Q

anxiety pathology and treatment related to seretonin pathway

A

Pathology: excessive amygdala activity (low 5HT activity). Treatment: increase 5HT activity (acutely) by 1. decreaseing termination (SERT): Fluoxetine-Venlafaxine. 2. Partial agonist at 5HT1a: Buspirone

47
Q

Roles of Diazepam-zolpidem, phenobarbital-alcohol, sevoflurane, flumazenil, baclofen, vigabatrin and tiagabine on the GABAergic pathway

A

Diazepam-zolpidem, phenobarbital-alcohol and sevoflurane are all GABAa agonists, Flumazenil is a GABAa antagonist, Baclofen is a GABAb agonist, Vigabatrin inhibits degradation and Tiagabine inhibits reuptak

48
Q

Seizure pathology and treatment related to GABA pathway

A

Pathology: depressed GABA activity leads to increased spread. Treament: GABA agonists: BDZs-Barbituates

49
Q

anxiety pathology and treatment related to GABA pathway

A

Pathology: excessive amygdala activity (low GABA activity). Treatment: GABA agonist: benzodiazepines

50
Q

Insomnia pathology and treatment related to GABA pathway

A

Path: excessive amygdala activity/decreased GABA activity. Treatment: GABA agonist: Z drugs (zolpidem)- benzodiazepam

51
Q

Anesthesia related to GABA pathway

A

Barbituates used to increase GABA

52
Q

Roles of lamotrigine, memantine, ketamine, alcohol on glutamatergic pathway

A

lamotrigine decreases release, memantine, ketamine, and alcohol are NMDA antagonists

53
Q

Alzheimers pathology and treatment related to glutamate pathway

A

Pathology: increased neuronal excitotoxicity
Treatment: decrease excitotoxicity via NMDA-R block: Memantine

54
Q

Pain pathology and treatment related to glutamate pathway

A

Pathology: abnormal neurotransmission in pain pathway. Treatment: decrease Glu activity via NMDA-R block: ketamine

55
Q

Seizure pathology and treatment related to glutamate pathway

A

Pathology: enhanced Glu activity leads to increased spread of excessive neuronal discharge. Treatment: decrease Glu release via VSCC block: Lamotrigine

56
Q

Anesthesia related to glutamate pathway

A

nitrous oxide decreases glut activity via NMDA-R block

Neuro unit 1 (17 decks)

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