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Pharmacology Exam I > Neurotransmitters > Flashcards

Neurotransmitters Flashcards

1
Q

What is a ligand?

A

a neurotransmitter, catecholamine, or drug that binds to a receptor and stimulates or inhibits some cellular function.

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2
Q

What do neurotransmitter signal transduction pathways depend on?

A

TYPE of receptor and WHERE receptor is, and WHICH neurotransmitter binds to it

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3
Q

Which 2 types of receptors are fast response receptors?

A

Ion receptors–ligand gated/voltage gated/other gated; and g-protein coupled receptors

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4
Q

Which 2 types of receptors are slow response receptors?

A

Enzyme linked transmembrane receptors and intracellular receptors.

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5
Q

Which receptor types are within the phospholipid membrane?

A

ligand gated, g-protein coupled, and enzyme linked transmembrane

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6
Q

Name types of ligand-gated ion channels.

A

Acetylcholine-neuromuscular blocking drugs, serotonin 5HT3, GABA-barbiturates and benzos, NMDA-ketamine and glycine receptors

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7
Q

Describe ligand gated ion receptors.

A

binding of the neurotransmitter causes a conformational change in the receptor which causes the ion channel to open or close. FAST RESPONSE. Examples: Nicotinic, NMDA, GABAa

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8
Q

Describe voltage sensitive ion channels.

A

gated by an ion, no ligand. Extracellular depolarization causing ions to flow. sodium, chloride, potassium, and calcium channels, depolarization causes ion flow through pores. in neurons, skeletal muscle and endocrine cells. LOCAL ANESTHETICS work here

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9
Q

Describe g-protein coupled receptors.

A

MOST ABUNDANT receptors in body, FAST, activates or inhibits an enzyme, ion channel, or other target receptor. Involves 2nd messengers. ex: hormones, catecholamines, opioids, anticholinergics, and antihistamines. ligand binds to a receptor, g-protein ignites effector protein involving intracellular messenger. ion shift or intracellular response

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10
Q

What is the difference between g-protein and ligand-gated receptors.

A

g-protein stimulate or inhibit intracellular messenger

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11
Q

Describe enzyme linked transmembrane receptors

A

SLOW, in luminal membrane, most are tyrosine kinases that use 2nd messenger. ex: insulin receptor, atrial natriuretic peptide, growth hormones.

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12
Q

Describe intracellular receptors.

A

SLOWEST, can cause response in or out of cell. ex: steroid receptors, thyroid hormone receptors, phosphodiesterase inhibitors.

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13
Q

Describe neurotransmitters and give examples.

A

secreted by neurons and act locally on other neurons. generally small organic molecules but polypeptides are larger. EX: acetylcholine, dopamine, NE, epi, histamine, serotonin, substance P, glutamate/aspartate, GABA/glycine

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14
Q

True/False: neurotransmitters produce the same effect in different locations depending on types of receptors present.

A

False. they produce DIFFERENT effects in different locations depending on types of receptors present.

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15
Q

Discuss acetylcholine synthesis.

A

AcetylCoA and choline are presynaptic and react with choline acetyltransferase to form acetylcholine.

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16
Q

Discuss acetylcholine degradation.

A

Acetylcholine and water combine with acetylcholinesterase and form acetic acid and choline. Acetate diffuses away and choline goes back to presynaptic neuron and reused to make more ACh.

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17
Q

How does acetylchoine work?

A

Exocytosis of ACh needed for signal transduction to occur. The basis for all interactions in the para and sympathetic nervous system.

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18
Q

Describe nicotinic receptors.

A

ligand-gated ion channel located between pre and post ganglionic neurons in para and sympathetic nervous system. ion channel opens allowing intracellular influx of Na+. located at NMJ, autonomic ganglia, and CNS.

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19
Q

What are nicotinic receptors stimulated by?

A

ACh, succinylcholine, and nicotine (not at NMJ)

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20
Q

What are nicotinic receptors blocked by?

A

NDMR (at NMJ) and trimethaphan (at autonomic ganglia)

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21
Q

Describe muscarinic receptors.

A

different from nicotinic; between post ganglionic and effector sites in 2 areas (1 para and 1 SNS), G-protein coupled. 5 subtypes M1-M5 located in CNS and organs of PNS. Includes 2nd messenger system.

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22
Q

What stimulates muscarinic receptors and what happens?

A

ACh and muscarine: salivary and sweat gland secretion, pupillary constriction, increases GI peristalsis, slows conduction of SA and AV nodes in heart (M2 receptor)

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23
Q

Where are receptors and neurotransmitters located?

A

between pre and post ganglia, no matter whether in SNS or PNS.

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24
Q

Where are catecholamines located?

A

between post ganglionic and effector cell, mainly SNS

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25
Q

Describe catecholamines and give examples.

A

synthesized by various neurons depending on the enzymes present. dopamine, epi, NE.

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26
Q

Where does dopamine act?

A

CNS neurons

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27
Q

Where does epi act?

A

second order neurons of SNS in adrenal medulla

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28
Q

Where does NE act?

A

second-order neurons of the SNS, adrenal medulla, and CNS neurons

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29
Q

Where is dopamine synthesized?

A

CNS, doesnt cross BBB

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30
Q

What are the 2 receptor classes for dopamine?

A

D1-like (D1 and D5) and D2-like (D2, D3, and D4)

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31
Q

What do D1-like receptors do?

A

increase cAMP

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32
Q

What do D2-like receptors do?

A

decrease cAMP

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33
Q

What are the central functions of dopamine?

A

Memory, problem-solving, reward-pleasure behavior, inhibition of prolactin secretion, fine control of movement, N/V CTZ.

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34
Q

What are the peripheral functions of dopamine?

A

coronary and renal vasodilation, higher serum concentrations affect beta-1 and alpha-1 receptors

35
Q

What are dopamine receptors are stimulated by?

A

dopamine and L-dopa

36
Q

What happens when dopamine receptors are agonized?

A

psychosis, euphoria, orthostatic hypotension, nausea

37
Q

What blocks dopamine receptors?

A

haldol, antipsychotics, antiemetics.

38
Q

What are the side effects of dopamine receptor antagonists?

A

parkinsonism, extrapyramidal reactions, hyperprolactinemia

39
Q

What terminates the action of dopamine?

A

diffusion away from the site, reuptake into pre-synaptic neuron, recycled and re-packaged, metabolized

40
Q

There are _____ major classes and _____ types of adrenergic receptors.

A

2; 5

41
Q

What are the types and classes of adrenergic receptors?

A

alpha-1, alpha-2, beta-1, beta-2, beta-3

42
Q

What terminates the action of norepi and epi?

A

diffusion away from the site, reuptake into the pre-synaptic neuron, recycled and repackaged, metabolized.

43
Q

What is histamine?

A

intrinsic neurotransmitter, synthesized from histadine in CNS (maintaining wakefulness), immune cells (basophils/mast cells), and GI tract (secreted by mast cells in stomach wall)

44
Q

How many types of Histamine receptors are there?

A

3

45
Q

Where are H1 receptors located?

A

vascular smooth muscle (dilation) and bronchial smooth muscle (contraction) and in CNS

46
Q

What are H1 antagonists?

A

diphenhydramine, loratidine

47
Q

Where are H2 receptors located?

A

stomach (increased acid secretion)

48
Q

What are H2 antagonists?

A

famotidine to increase gastric pH

49
Q

Where are H3 receptors located?

A

presynaptic reduction in further histamine release. negative feedback loop, don’t send more histamine

50
Q

Where is serotonin (5-hydroxytryptamine) found and what does it do?

A

intestine–regulates intestinal movement; raphe nucleus in brainstem and projects to other regions of the brain to affect mood, cognition, sleep

51
Q

How many families of serotonin receptors are there?

A

7

52
Q

What type of receptor are the serotonin receptors 5-HT1,2,4,5,6,7?

A

g-protein coupled

53
Q

What type of receptor is 5-HT3?

A

ligand gated Na and K cation channel. Depolarizes plasma membrane, excitatory, only type that is ionotropic.

54
Q

What does 5-HT3 cause?

A

nausea

55
Q

What are other effects of serotonin?

A

addiction, aggression, vasoconstriction, increased intestinal motility, learning and memory consolidation

56
Q

What are some serotonin agonists?

A

busiprone: anxiety; triptans: migraines; LSD, psilocin: psychedelic drugs; cisapride: increases GI motility

57
Q

What are some serotonin antagonists?

A

ondansetron, risperidone: antipsychotic

58
Q

What is substance P’s claim to fame?

A

primary neurotransmitter produced by pain/temp afferent peripheral neurons

59
Q

What are the substance P receptors?

A

neurokinin receptors (NK1, NK2, NK3)

60
Q

Where else are substance P receptors located?

A

gut/CTZ–nausea/emesis pathways

61
Q

What does blocking Substance P do?

A

reduce N/V

62
Q

What neurotransmitters are associated with PONV?

A

dopamine, serotonin, acetylcholine, Histamine, (opioids), Substance P

63
Q

What is the primary brain excitatory neurotransmitter?

A

Glutamate, most prominent in brain

64
Q

What is the primary spinal cord excitatory neurotransmitter?

A

aspartate

65
Q

Does glutamate cross the BBB?

A

No, it’s charged

66
Q

How is glutamate synthesized?

A

from glutamine (which does cross the BBB)

67
Q

What is an important Glutamate Receptor?

A

NMDA receptor (an ionotropic receptor)

68
Q

Describe an NMDA receptor.

A

N-methyl-d-aspartate receptor, non-specific cation channel, Na and Ca enter cell and K leaves the cell resulting in neuronal depolarization.

69
Q

What is required to activate an NMDA receptor?

A

glutamate AND glycine

70
Q

What are some NMDA receptor antagonists?

A

dextromethorphan, Ketamine, N2O, Mg, methadone

71
Q

What is the primary inhibitory neurotransmitter in the brain?

A

GABA (gamma amino butyric acid).

72
Q

What is the 2nd most abundant neurotransmitter in the brain?

A

GABA

73
Q

What is the primary inhibitory neurotransmitter in the spinal cord?

A

glycine

74
Q

Where is GABA synthesized?

A

pre-synaptic neuron from glutamate, the primary excitatory neurotransmitter is converted to the primary inhibitory neurotransmitter.

75
Q

What type of receptors are GABAa receptors?

A

ionotropic ligand-gated ion channels

76
Q

How does a GABAa receptor work?

A

allows passage of Cl- from extracellular to intracellular and the increased intracellular Cl- leads to hyperpolarization of the neuron causing it to be less likely to fire

77
Q

Define allosteric regulation.

A

drug or chemical binds to a receptor at a site different from primary site and alters regulation of action of receptor’s primary agonists and antagonists. can increase receptors affinity for its primary neurotransmitter or decrease the affinity.

78
Q

What do positive allosteric modulators do?

A

enhance the affinity of the receptor for GABA

79
Q

Name some positive allosteric modulators.

A

barbiturates, propofol, etomidate, benzos, steroids

80
Q

Name some negative allosteric modulators

A

Flumazenil. decrease the action of GABA at this receptor

81
Q

What type of receptors are GABAb receptors?

A

g-protein

82
Q

What do GABAb receptors do?

A

cause intracellular changes resulting in opening of K channel, K leaves neuron resulting in neuronal hyperpolarizaiton aka inhibition.

83
Q

What are some GABAb agonists?

A

baclofen, gamma hydroxybutyrate, ecstasy, date rape drug

84
Q

The practice of anesthesia involves the manipulation of neurotransmitters in both _______ and ________.

A

health and disease.

Pharmacology Exam I (11 decks)

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