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Neuro Exam #1 > CNS neuropharmacology > Flashcards

CNS neuropharmacology Flashcards

1
Q

what is the hypothalamus responsible for?

A

sleep, appetite, endocrine

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2
Q

What is the thalamus responsible for?

A

pain, sensory relay to and from cortex, alertness

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3
Q

what is the hippocampus responsible for?

A

memory, reexperiencing

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4
Q

what is the amygdala responsible for?

A

fear, anxiety, panic

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5
Q

what is the basal forebrain responsible for?

A

memory, alertness

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6
Q

what is the striatum responsible for?

A

motor, critical relay site from PFC

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7
Q

what is the nucleus accumbens responsible for?

A

delusions, hallucinations, pleasure, interests, libido, fatigue, euphoria, reward, motivation

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8
Q

what is the prefrontal cortex responsible for?

A

executive function, attention, concentration, emotions, impulses, obsessions, compulsions, motor, fatigue, ruminations, worry, pain, negative symptoms, guilt, suicidality.

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9
Q

what are relay neurons?

A

neurons that form interconnecting pathways in order to transmit signals over long distances. they have large cell bodies and their axons project over long distances, but they also have smaller collaterals that synapse on local interneurons. They are *excitatory, releasing glutamate, and activating ionotropic receptors.

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10
Q

what are local circuit neurons?

A

smaller neurons that branch in immediate vicinity of cell body. They synapse primarily on cell bodies of relay neurons. Commonly use feed-forward and recurrent feedback pathways. In the spinal cord a special class forms axoaxonic synapses on terminals of sensory relay neurons. They are mostly inhibitory, releasing GABA.

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11
Q

what are hierarchical systems?

A

neuronal systems with clearly delineated pathways directly involved in motor control and sensory perception. Composed of large myelinated neurons and rapid conduction velocity. information is processed sequentially and integrated successively at relay nuclei.

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12
Q

6 key neurotransmitter systems targeted by psychopharmacologic agents

A

GABA, Glu, ACh, DA, NE, 5-HT

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13
Q

Diffuse systems

A

neural systems that modulate hierarchical systems. There are few that they have wide and difusse projections throughout the brain. Can affect vast CNS areas simultaneously subserving global functions such as attention, sleep-wake cycle, appetite, emotions.

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14
Q

monoamines

A

dopamine, NE, 5-HT

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15
Q

how is GABA synthesized?

A

formed from glutamate via GAD

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16
Q

how is GABA action terminated?

A

reuptake. transported back into presynaptic nerve terminal via GABA transporter.

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17
Q

MOA of benzos

A

Facilitate GABA action by increasing frequency of Cl- channel opneing. Most have long half-lives and active metabolites.

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18
Q

MOA of tiagabine

A

GABA reuptake inhibitor.

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19
Q

MOA of vigabatrin

A

inhibits degradation of GABA-Tramsaminase/GABA-T

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20
Q

GABAa mechanism

A

ionotropic. opens ligand-gated Cl- channel, which decreases neuronal excitability.

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21
Q

GABAb mechanism

A

Gi/o. inhibits adenylyl cyclase, decrease Ca conductance, opens K+ channel.

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22
Q

where are GABA receptors located?

A

high concentrations in brain and spinal cord.

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23
Q

why does GABA play a pathophysiological role in?

A

decreased in anxiety and HD. also in seizure disorders, sleep disorders, alcohol abuse and withdrawal.

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24
Q

how is glutamate synthesized?

A

interaction between nerve terminals and glial cells. Glutaminase froms glutamate from glutamine.

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25
Q

What happens to glutamate after it’s released?

A

1) reuptake 2) taken up by glial cell transporter and converted to glutamine by glutamine synthetase.

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26
Q

receptors for glutamate

A

ionotropic + metabotropic

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27
Q

ionotropic receptors for glutamate

A

NMDA (increase Ca++ influx), AMPA (increase Na and Ca influx), Kainate (increases Na influx)

28
Q

metabotropic receptors for glutamate

A

R1-R5 (Gq–> increase PLC activity), R2-R3 (Gi/o –> decrease AC activity - activate K+ channels), R4-R6-R7-R8 (Gi/o–> inhibits AC, inhibit VSCC)

29
Q

location of glutamate?

A

present on virtually all neurons in CNS, highest in hippocampus, cortex, lateral septum, striatum, and cerebellum

30
Q

function of glutamate?

A

mediates vast majority of excitatory synaptic transmission in the CNS, triggers neuroplasticity. when overactivated can trigger excitotoxicity.

31
Q

pathophys role of glutamate?

A

epilepsy, ischemic brain damage, addiction, schizophrenia.

32
Q

how is ACh synthesized?

A

catalyzed by choline acetyl transferase

33
Q

how is ACh stored?

A

VAT, vesicle-associated transporter stores it and packages it.

34
Q

action of muscarinic receptors for ACh?

A

M1-M3: Gq –> stimulate PLC activity. M2-M4: Gi/o –> inhibit adenylyl cyclase activity

35
Q

CNS location of ACh?

A

cell bodies in brain stem and basal forebrain that project to the cerebral cortex and hippocampus. More specifically, MSN (medial septal nuclei), DB (diagonal band of Broca), Ch5-Ch8: cholinergic brainstem nuclei.

36
Q

Function of ACh

A

coordinated movement and cognitive functions (motivation, memory, and learning)

37
Q

pathophys role of ACh?

A

AD, PD, schizoprenia

38
Q

catecholamines

A

dopamine, NE

39
Q

what is the rate-limiting enzyme for catecholamine synthesis?

A

tyrosine hydroxylase (TH)

40
Q

what is the rate-limiting enzyme for 5HT synthesis?

A

tryptophan hydroxylase (TpH)

41
Q

monoamine storage?

A

VMAT, vesicular monoamine transporter packages it, stores it, and protects it from degradation by MAO.

42
Q

reserpine

A

VMAT inhibitor, so it blocks monoamine vesicular uptake and increases degradation by MAO. net effect = decreased monoamine release and action.

43
Q

phenelzine-selegiline

A

MAOIs. this decreases MAO degradation and increases vesicular storage, resulting in increased monoamine release and action.

44
Q

how are monoamines terminated?

A

primarily REUPTAKE. once in the cytosol, either 1) inactivated by MAO or 2) transported into the vesicle by VMAT.

45
Q

NE action on alpha1

A

Gq: stimulation of phospholipase C

46
Q

NE action on alpha2

A

Gi/o: inhibition of adenylyl cyclase activity K+ channel opening

47
Q

NE action on beta1/beta2

A

stimulation of adenylyl cyclase

48
Q

dopamine transduction mechanism

A

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

49
Q

serotonin action on 5HT4

A

Gs –> stimulation of adenylyl cyclase

50
Q

serotonin action on 5HT3

A

ligand-gated cation channel - excitatory

51
Q

serotonin action on 5HT2A,2B,2C

A

Gq–> phospholipase C - closing of Ca channel

52
Q

serotonin action on 5HT1A,1B,1D

A

Gi/o –> inhibition of adenylyl cyclase activity and opens K+ channel.

53
Q

dopamine CNS location?

A

substantia nigra, ventral tegmental area

54
Q

NE CNS location?

A

cell bodies in pons and brain stem (locus ceruleus) proejcting to all brain levels. More specifically, A1,A2,A5,A7 adrenergic brainstem nuclei.

55
Q

Serotonin CNS location?

A

raphe nuclei in pons/upper brain stem that project to all levels of brain

56
Q

function of dopamine?

A

initiation of voluntary movement, reward-related behaviors, working memory, attention

57
Q

NE function?

A

arousal, attention, vigilance, sleep-wake cycle, fear response, anxiety, mood/emotion, afferent pain signals

58
Q

serotonin function?

A

sleep, arousal, attention, sensory information in cerebral cortex, emotion/mood regulation, pain, eating/drinking behaviors

59
Q

pathophys role of dopamine

A

Increased in HD, decreased in PD and depression. Also schizophrenia, OCD, ADHD, drug abuse.

60
Q

pathophys role of NE

A

Increased in anxiety, decreased in depression. Also mania, PTSD, panic attacks, ADHD

61
Q

pathophys role of serotonin

A

decreased in depression and anxiety. schizophrenia, eating disorders

62
Q

Where is NE synthesized?

A

llocus ceruleus (pons)

63
Q

Where is dopamine synthesized?

A

ventral tegmentum and substantia nigra pars compacta (midbrain)

64
Q

Where is 5-HT synthesized?

A

Raphe nuclei (pons,medulla,midbrain)

65
Q

Where is ACh synthesized?

A

Basal nucleus of Meynert

66
Q

Where is GABA synthesized?

A

Nucleus accumbens

Neuro Exam #1 (23 decks)

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