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Neuroscience > Neuroscience Week 2: Neurotransmitters > Flashcards

Neuroscience Week 2: Neurotransmitters Flashcards

1
Q

Classes of Neurotransmitters

6 listed

A
  • Acetylcholine
  • Biogenic Amines
  • Amino Acids
  • Peptides
  • Purines
  • Gases and Lipids
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2
Q

Direct Neurotransmitters

A

Bind to ion channels and open them

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3
Q

Indirect Neurotransmitters

A

signal through second messenger pathways (G-protein)

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4
Q

Biogenic Amines Examples

A

Dopamine

Serotonin

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5
Q

Neurotransmitters: Amino Acid examples

A

GABA

Glutamate

Glycine

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6
Q

Neurotransmitters: Peptides examples

A

Endorphins

Substance P

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7
Q

Neurotransmitters: Purines examples

A

ATP

Adenosine

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8
Q

Neurotransmitters: Gases and Lipids examples

A

Nitric oxide

Endocannabinoids

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9
Q

Identify

A
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10
Q

Anterograde transport is in which direction

A

Away from the cell body

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11
Q

Retrograde transport is in which direction

A

Toward the cell body

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12
Q

Anterograde and retrograde transport speeds

A
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13
Q

Anterograde and retrograde transport Caveats

A
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14
Q

Some acetylcholinesterase inhibitors

A
  • Pyridostigmine (M. Gravis)
  • Donepezil (Alzheimer’s)
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15
Q

Ach Neurotransmission

A
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16
Q

Nicotinic Receptors AKA

A

Excitatory

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17
Q

Muscarinic Receptors AKA

A

Mixed

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18
Q

Nicotinic Receptors Function

A

Cation permeable channel (ionotropic)

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19
Q

Nicotinic Receptors Location

A
  1. NMJ
  2. Autonomic ganglia
  3. CNS
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20
Q

Nicotinic Receptors Competitive Antagonist

A

Tubocurarine

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21
Q

Nicotinic Receptors Effect of ACh cholinesterase inhibition

A

Activation

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22
Q

Muscarinic Receptors Effect of ACh cholinesterase inhibition

A

Activation

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23
Q

Muscarinic Receptors Effect Competitive Antagonist

A

Atropine

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24
Q

Muscarinic Receptors Location

A
  1. Parasympathetic
  • Myocardium (M<span>2</span>: G<span>i</span> coupled; ↓cAMP)
  • Smooth muscle (M1: Gq coupled; ↑Ca2+)
  1. CNS
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25
Q

Muscarinic Receptor Function

A

G Protein-coupled receptor (metabotropic)

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26
Q

ACh receptor overview

A
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27
Q

Identify

A
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28
Q

Basal Nucleus of Meynert is damaged in?

A

Alzheimer’s Disease

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29
Q

Identify

A
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30
Q

Identify

A
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31
Q

Overview

A
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32
Q

Overview of Pharmacology of Neuromuscular Blocking Agents

A
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33
Q

Non-Depolarizing Competitive Antagnoists Examples

A

Isoquinalines:

  • d-Tubocurarine
  • atracurium

Steroids:

  • Pancuronium
  • Rocuronium
  • vecuronium
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34
Q

Non-Depolarizing Competitive Antagnoists timing of Action

A

Onset 90 sec

duration 20-50 minutes

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35
Q

Non-Depolarizing Competitive Antagnoists elimination

A

Spontaneous (hydrolysis)

Kidney and/or liver

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36
Q

Non-Depolarizing Competitive Antagnoists Uses

A

Surgical relaxation

endotracheal intubation

control of ventilation (ICU)

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37
Q

Non-Depolarizing Competitive Antagnoists Adverse Effects

A

hypotension and bronchoconstriction due to histamine release

tachycardia

prolonged paralysis

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38
Q

Non-Depolarizing Competitive Antagnoists Reversal of blockade

A

cholinesterase inhibitors

Sugammedex (modified gamma-cyclodextrin-for steroid derivatives)

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39
Q

Non-Depolarizing Competitive Antagnoists Interactions

A

NMJ blockade is potentiated by volatile general anesthetics and antibiotics (aminoglycosides)

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40
Q

Depolarizing Agonists MOA

A

Phase 1: depolarizing block of Na+ channels (inactivation gate closes)

Phase 2: Desensitization (nAChR in closed state)

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41
Q

Depolarizing Agonists Examples

A

Succinylcholine

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42
Q

Depolarizing Agonists Timing

A

Onset 30 sec

duration < 8 min

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43
Q

Depolarizing Agonists elimination

A

Plasma and liver cholinesterases (insensitive to synaptic acetylcholinesterase)

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44
Q

Depolarizing Agonists Uses

A
  • Surgical relaxation
  • Endotracheal entubation
  • Control of ventilation (ICU)
  • Aid in treatment of convulsions or electroconvulsive therapy (Succinyl-Ch)
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45
Q

Depolarizing Agonists Adverse effects

6 listed

A
  • Rhabdomyolysis
  • myalgias
  • hyperkalemia
  • hypercalcemia
  • ↑ intraocular pressure
  • ↓ heart rate due to muscarinic effects
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46
Q

Depolarizing Agonists Reversal of blockade

A

Stop infusion (rapid elimination)

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47
Q

Depolarizing Agonists Interactions

A

Malignant hyperthermia is a rare complication when used in conjunction with volatile anesthetics

End-plate depolarizing effect can be blocked by nondepolarizing agent

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48
Q

Transdermal electrical stimulation

A
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49
Q

conditions that have the potential to up-regulate acetylcholine receptors

6 listed

A

potential for hyperkalemia with succinylcholine

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50
Q

conditions that have the potential to up-regulate acetylcholine receptors

6 listed

& Effects

A
  • increased resistance to non-depolarizing
  • hyperkalemia after succinylcholine
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51
Q

conditions that have the potential to down-regulate acetylcholine receptors

3 listed

A
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52
Q

Myasthenia Gravis Etiology

A
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53
Q

Myasthenia Gravis Age of Presentation

A
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54
Q

Myasthenia Gravis Clinical Presentation

A
55
Q

Myasthenia Gravis Associated with

A
56
Q

Myasthenia Gravis Laboratory Tests

A
57
Q

Myasthenia Gravis Treatment

A
58
Q

Lambert-Eaton Etiology

A
59
Q

Lambert-Eaton Age of Presentation

A
60
Q

Lambert-Eaton Clinical Presentation

A
61
Q

Lambert-Eaton Associated with

A
62
Q

Lambert-Eaton Laboratory Tests

A
63
Q

Lambert-Eaton Treatment

A
64
Q

Botulism Etiology

A
65
Q

Botulism Age of Presentation

A
66
Q

Botulism Clinical Presentation

A
67
Q

Botulism Associated With

A
68
Q

Botulism Laboratory tests

A
69
Q

Botulism Treatment

A
70
Q

OPMD Etiology

A
71
Q

OPMD Age of presentation

A
72
Q

OPMD Clinical Presentation

A
73
Q

OPMD Associated With

A
74
Q

OPMD Laboratory Tests

A
75
Q

OPMD Treatment

A
76
Q

GABA Pathway

A
77
Q

Pyridoxine Deficiency

A

Pyroxidine (Vitamin B6) deficiency may occur in patients without adequate dietary intake can cause seizures

certain conditions can be risky for B6 deficiency despite adequate dietary intake include the elderly patients undergoing dialysis, patients with liver disease, and pregnant women

78
Q

Some anti-epileptic drugs can modulate

A

GABA release

79
Q

Closed loop GABA pathway is called

A

GABA Shunt

80
Q

GABA Receptor Types

A
  • GABAA
  • GABAB
81
Q

GABAA Function

A

anion permeable channel (ionotropic)

82
Q

GABAA Location

A

All CNS (Glycine receptors are also anion permeable; mediated inhibition in the brain stem and spinal cord antagonized by strychnine)

83
Q

GABAA ​Clinical Importance Diseases

A
  • anxiety and sleep disorders
  • Seizures
  • Detox (alcohol withdrawal)
  • Surgical conditions and critical care
84
Q

GABAA ​Drug (potentiators)

A
  • Anxiolytics, sedatives, hypnotics (e.g. benzodiazepines)
  • Anti-convulsants (e.g. phenobarbital)
  • Benzodiazepines
  • General anesthetics (e.g. propofol)
85
Q

GABAA Importance in other diseases

A
  • Huntington’s Disease
  • Hepatic encephalopathy
86
Q

GABAA Pharmacology pneumonics

A

Benzodiazepines increase frequency of channel opening = frenzodiazepines

Barbituates the duration of openings = barbidurates

87
Q

GABAB Function

A

G protein-coupled receptor (metabotropic)

88
Q

GABAB Location

A

All CNS

89
Q

GABAB Clinical Importance Diseases

A
  • Spasticity
  • Substance use disorder
90
Q

GABAB Clinical Importance Drug

A
  • Spasmolytic agents (e.g. baclofen)
  • gamma-hydroxybutyric acid (GHB)
91
Q

GABAB Dual Mechanism of Action

A

has a dual mechanism of action:

1) presynaptically, inhibit Ca2+ channels, reducing transmitter release
2) postsynaptically, potentiate K+ channels, hyperpolarizing membrane potential

92
Q

Glutamate pathway

A
93
Q

Glutamate release is modulated by some?

A

Anti-epileptic drugs and riluzole (used for amyotrophic lateral sclerosis)

94
Q

Glutamate Receptors

A
  • NMDA (Excitatory)
  • AMPA (Excitatory)
95
Q

NMDA Receptor Function

A
  • Cation permeable channel (ionotropic)
  • Ca2+ permeable (excitotoxicity)
  • Requires both glutamate and glycine for activation
  • Blocked by Mg2+ at negative membrane potentials
  • Involved in learning and memory
96
Q

NMDA Receptor Location

A

All CNS

97
Q

NMDA Receptor Clinical Importance

A
98
Q

AMPA Receptor Function

A
  • Cation permeable channel (ionotropic)
  • activated by glutamate alone at negative membrane potentials (excitotoxicity)
  • Involved in learning and memory
99
Q

AMPA Receptor Location

A

All CNS

100
Q

AMPA Receptor Clinical importance

A

Epilepsy -> Perampanel (anti-convulsant)

101
Q

NMDA Mg2+ Block

A
102
Q

Postsynaptic Integration

A
103
Q

EPSP

A

Excitatory post-synaptic potential depolarizes and makes an action potential more likely

104
Q

IPSP

A

Inhibitory post-synaptic potential is inhibitory and hyperpolarizes making an action potential less likely

105
Q

Synaptic potentiation

A

Continuous synapse use enhances stimulation

106
Q

Presynaptic inhibition

A

Release of neurotransmitter blocked by another neuron’s axoaxonal synapse

107
Q

Temporal Summation

A

Neuron signals close together in time

108
Q

Spatial summation

A

multiple simultaneous stimulations at different locations

109
Q

summary of neurotransmitters

A
110
Q

Catecholamine synthesis

A
111
Q

Serotonin and melatonin synthesis

A
112
Q

Question 1

A
113
Q

Question 2

A
114
Q

Question 3

A
115
Q

Question 4

A
116
Q

Question 7

A
117
Q

Question 8

A
118
Q

Question 9

A
119
Q

Question 10

A
120
Q

Question 11

A
121
Q

Question 12

A
122
Q

Question 13

A
123
Q

Question 14

A
124
Q

Question 15

A
125
Q

Question 16

A
126
Q

Question 17

A
127
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Question 18

A
128
Q

Question 19

A
129
Q

Question 20

A
130
Q

Question 21

A
131
Q

Question 22

A
132
Q

Question 23

A
133
Q

antagonized by strychnine

A

Glycine Receptors

Neuroscience (96 decks)

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