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Drugs & Behavior > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

what is a property of ligands and their receptors?

A

ligands can bind to multiple receptors

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2
Q

what are the two types of ligand receptors?

A

metatropic and ionotropic
-meta: channel and binding site DIFFERENT proteins, GTP
-iono: channel and binding site SAME protein

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3
Q

what are the 6 criteria to be a monoamine?

A
  1. NT are in the axon terminals
  2. NT is released by action potentials
  3. present in NT postsynaptic receptors
  4. must have a mechanism for termination (inactivation)
  5. external application mimics normal response
  6. receptor antagonist inhibits effects of NT and presynaptic stimulation
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4
Q

what are the two different forms of monoamines (MA)?

A

catecholamines and indolamine

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5
Q

whats the difference b/w a catecholamine and an indolamine?

A

catechol: 1 ring, tyrosine precursor
indole: 2 rings, tryptophan precursor

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6
Q

where are monoamines found and how many are there?

A

in the CNS (midbrain, pons, medulla)
-about 1 million

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7
Q

what NT are under the class catecholamines?

A

dopamine (DA)
norepinephrine (NE): nonradrenergic and adrenergic forms
epinephrine (EPI): adrenergic form

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8
Q

what NT are under the class indolamines?

A

serotonin (5-HT)
melatonin (MT)

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9
Q

what is the overall way monoamines are terminated?

A

presynaptic reuptake via active transport
-in the liver

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10
Q

what are the two distinct ways monoamines are terminated?

A

-monoamine oxidase (MAO)
-catechol-O-methyltransferase (COMT)

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11
Q

what NT does MAO terminate and where?

A

ALL: DA, NE, 5-HT
-in axon terminal and astrocytes

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12
Q

what NT does COMT terminate and where?

A

catechol only: DA, NE
-in astrocytes and microglia

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13
Q

what does Reserpine do to monoamines?

A

decrease NT storage by blocking the MA transporter VMAT2
-NT is degraded by MAO in axon terminal
-indirect ANT

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14
Q

what does MAOI (monoamine oxidase inhibitor) do to monoamines?

A

blocks MAO from degrading NT
-indirect agonist

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15
Q

what do reuptake blockers do to monoamines?

A

increase NT in the synapse
-antidepressants, cocaine, amphetamine

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16
Q

what are examples of action potential independent DA and NE release?

A

amphetamine and methamphetamine

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17
Q

where does dopamine come from?

A

midbrain in the CNS

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18
Q

what are the three ascending pathways of dopamine?

A

Nigrostriatal Pathways
Mesolimbic Pathway
Mesocortical Pathway

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19
Q

what is the nigrostriatal pathway?

A

substantia nigra -> striatum
-deals with movement (Parkinson’s)

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20
Q

what is the mesolimbic pathway?

A

ventral tegmental area (VTA) -> limbic
-deals with addiction (schizophrenia)

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21
Q

what is the mesocortical pathway?

A

VTA -> cortex
-deals with addiction (schizophrenia)

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22
Q

how many dopaminergic types are there?

A

5 (DA-R)

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23
Q

are DA-R metabotropic or ionotropic?

A

metabotropic

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24
Q

what are the two main classes of DA-R and what do they do?

A

D1 family (D1 & D5): activates GS, increase cAMP
D2 family (D2, D3, D4): activates GI, decreases cAMP, opens K+ channels

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25
Q

what are examples of dopaminergic agonists and antagonists?

A

agonist: L-DOPA (Tx for Parkinson’s)
ANT: Thorazine (D1), Haldol (D2)

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26
Q

what is the synthesis of dopamine and what are the enzymes?

A

tyrosine –(tyrosine hydroxylase)–> DOPA –(aromatic AA decarboxylase)–> DA

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27
Q

what is the major metabolite of DA and what does a major metabolite do?

A

homovanillic acid (HVA)
-you can check levels of the major metabolite in the CSF fluid to monitor levels of the NT

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28
Q

where does norepinephrine (NE) come from?

A

mainly the adrenal glands of the PNS (from sympathetic receptors)
-can also come from the locus coeruleus of the CNS

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29
Q

what is the receptor for NE and what are the types?

A

Adrenergic Receptors
-alpha-adrenoceptor
-beta-adrenoceptor

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30
Q

what do alpha-adrenoceptors do?

A

alpha1: Gq, increases Ca2+
alpha2: GI, decrease cAMP, opens K+ channel

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31
Q

what do beta-adrenoceptors do?

A

B1 and B2
-Gs, increase cAMP

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32
Q

what are examples of adrenergic agonists and antagonists?

A

agonists: ephedrine, mescaline
ANT: propranolol (beta blocker)

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33
Q

what receptor does epinephrine bind to and what is it made from?

A

same adrenergic receptors as NE
-synthesized from NE

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34
Q

what is the synthesis of NE and what are the enzymes?

A

tyrosine –(tyrosine hydroxylase)–> DOPA –(AADC)–> DA –(dopamine beta hydroxylase)–> NE

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35
Q

what are the NE major metabolites?

A

MHPG and VMA

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36
Q

where does serotonin (5-HT) come from?

A

the raphe nuclei in the PNS
-in the midline of the brain stem (dorsal and median)

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37
Q

what are the functions of serotonin?

A

breathing, eating, pain modulations, anxiety, learning, memory

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38
Q

how many receptor types are there in 5-HT?

A

7 types with subtypes within each type

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39
Q

are 5-HT receptors metabotropic or ionotropic? what is the exception?

A

metabotropic
-EXCEPT 5-HT3

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40
Q

what are the 5-HT agonists?

A

MDMA (Ecstasy): neurotoxicity
LSD: in 8 receptor types, 5-HT2a (hallucinations)
Phenethylamines: mescaline
Buspirone (Buspar): anxiolytic (Tx anxiety), 5-HT1a

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41
Q

what are the 5-HT inverse agonists?

A

Ketanserin: 5-HT2, decrease 2nd messenger systems

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42
Q

what are the 5-HT antagonists?

A

Risperidone: antipsychotic, 5-HT2a

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43
Q

what is the synthesis of 5-HT?

A

tryptophan –(tryptophan hydroxylase)–> 5-HTP –(AADC)–> 5-HT

5-HTP: hydroxytryptophan
5-HT: hydroxytryptamine

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44
Q

what is the major metabolite of 5-HT?

A

5-HIAA (hydroxyindoleacetic acid)

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45
Q

is acetylcholine (ACh) a type of monoamine?

A

NO

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46
Q

what is the ACh precursor?

A

choline (comes from fat in our diet)

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47
Q

what enzyme degrades ACh?

A

acetylcholinesterase (AChE)
-inside the presynaptic cell and on postsynaptic membrane

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48
Q

what are the two receptor types in ACh and what type of ligand receptor are they?

A

nicotinic (ionotropic)
muscarinic (metabotropic)

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49
Q

what is the synthesis of ACh?

A

choline + acetyl CoA –(choline acetyltransferase)–> ACh

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50
Q

what are the characteristics of nicotinic receptors (nACh-R)?

A

MULTIPLE SUBUNITS and RECEPTOR SUBUNITS
-excitatory: control Na+ and Ca2+ channels
-desensitizes: inactive and becomes active spontaneously
-depolarization block: w/ continuous stimulation, it reaches a max and impairs the action potential

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51
Q

what are the characteristics of muscarinic receptors?

A

5 TYPES (M1-M5)
-excitatory or inhibitory
-controls 2nd messenger systems: decreases cAMP, increases phosphoinositide activity
-G-protein coupled channel: opens K+ channel

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52
Q

what three areas is ACh distributed in the PNS and what receptor subtype are they?

A

-skeletal muscle: NICOTINIC
-autonomic ganglia: NICOTINIC
-parasympathetic neuroeffector: MUSCARINIC

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53
Q

what four areas is ACh distributed in the CNS and what receptor subtype are they? What are their functions?

A

all MUSCARINIC
-neocortex and hippocampus: memory
-striatum: movement
-lateral dorsal tegmentum: reward
-basal forebrain (BFCS): conscious arousal

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54
Q

what are ACh direct agonists?

A

-muscarine
-nicotine (low dose stimulates)
-succinylcholine (nACh-R, degradation resistant, muscle relaxant)

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55
Q

how is AChE inhibited?

A

indirectly through irreversible binding and reversible binding

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56
Q

AChE inhibition through irreversible binding

A

-ANTAGONIST
-binds AChE so long it can’t work fast enough to replace it
-sarin and soman (nerve gases)

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57
Q

AChE inhibition through reversible binding examples

A

pyridostigmine: used during war to protect against gases
physostigmine: Tx for glaucoma and myasthenia gravis
neostigmine: Tx for myasthenia gravis

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58
Q

ACh direct antagonists (nicotinic and muscarinic) examples

A

NICO: curare (paralysis at muscle)
MUSC: atropine (antidote for nerve gas), scopolamine (antinausea)

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59
Q

ACh indirect antagonists (decreases ACh)

A

hemicholinium: blocks choline receptor
Botulinum Toxin: cleaves SNAREs, prevents vesicular membrane fusion
Black Widow Venom: increase of Ca2+ (influx)

60
Q

what are unmodified AA?

A

includes nonessential AA (not form our diet)
-form peptides

61
Q

what are the two excitatory AA?

A

work at receptors that excite, are NOT excitatory THEMSELVES!!
-glutamate (Glu)
-aspartate (Asp)

62
Q

what are the two inhibitory AA?

A

GABA
glycine (Gly)

63
Q

where is glutamate found?

A

only in the CNS

64
Q

what is glutamate synthesized from?

A

glutamine (comes from astrocytes)

65
Q

is glutamate released on its own?

A

no, its co-released with other NT (ACh, DA, 5-HT, GABA)

66
Q

what are the three types of ionotropic glutamatergic receptors?

A

AMPA-R: Na+ influx
Kainate-R: Na+ influx
NMDA-R: Na+ and Ca2+ influx (hybrid receptor)

67
Q

what are do metabotropic glutamatergic receptors do?

A

-decrease cAMP
-increase phosphoinositide activity

68
Q

where is glutamate distributed? (3)

A

Cerebral Cortex: pyramidal neurons
Hippocampus: LTP, LTD
Cerebellum: LTD

69
Q

why can glutamate only be distributed in these three areas?

A

it can’t cross the BBB

70
Q

what is excitotoxicity?

A

when a brain injury occurs, it increases glutamate
-leads to programmed cell death

71
Q

what is the full name of GABA and is it an AA?

A

gamma-aminobutyric acid
-NOT an AA, only a NT

72
Q

what is GABA synthesized from?

A

glutamate

73
Q

what degrades GABA?

A

GABA-aminotransferase (GABA-T)

74
Q

what are the two receptors for GABA?

A

GABA(a)
GABA(b)

75
Q

characteristics of GABA(a)

A

-ionotropic
-Cl- influx which creates an IPSP
-allosteric binding

76
Q

characteristics of GABA(b)

A

-metabotropic
-decreases cAMP
-opens K+ channel

77
Q

how is GABA synthesized and what are the enzymes?

A

Glutamine –(glutaminase)–> Glutamate –(glutamic acid decarboxylase)–> GABA

78
Q

what are examples of GABAergic agonists, antagonists, and inverse agonists?

A

agonist: benzodiazepines, barbiturates, ethyl alcohol
ANT: picrotoxin
inverse agonist: beta carboline-3-carboxylate (produces anxiety)

79
Q

what are neuropeptides and where are they synthesized?

A

chains of AA
-neuromodulation
-synthesized in the soma

80
Q

what are two common examples of neuropeptides?

A

-substance P
-endorphins

81
Q

what are endorphins?

A

-produce analgesia (w/o pain) and euphoria :)
-co-released with NT’s
-bind at opioid receptors

82
Q

what are the opioid receptor classes? (4)

A

-dynorphin
-met- and leu- enkephalins
-beta endorpin
-endomorphins

83
Q

what are the four opioid receptor subtypes?

A

-mu (µ), delta (δ), kapa (κ)
-nociceptin/orphanin FQ receptor (nalozone insensitive)

84
Q

direct agonist and direct ANT of endorphins?

A

agonists: morphine, codeine, heroin
ANT: naloxone, naltrexone

85
Q

what does histamine do?

A

-inflammatory response
-conscious arousal

86
Q

what do purines do?

A

-co-released from vesicles
-movement
-make sensory and autonomic ganglia

87
Q

what do retrograde messengers do?

A

send message from postsynaptic cell to presynaptic cell
-Ca2+ dependent release
-not stored in vesicle (highly lipid soluble)
-types: (NO), endocannabinoids

88
Q

how is nitric oxide (NO) synthesized?

A

(NO) synthase

89
Q

what do endocannabinoids do, how are they synthesized, and what are the two types?

A

-inhibit presynaptic GABA release
-synthesized through degradation of membrane
-types: anandamide, 2-AG (arachadonoylglycerol)

90
Q

how did the autonomic NS get its name?

A

b/c the effectors are autonomous
-don’t need a neural input to function

91
Q

where in the body do autonomic NS control?

A

smooth muscle, cardio muscle, glands

92
Q

what class of drugs impacts the autonomic NS?

A

psychoactive drugs

93
Q

what type of regulation is homeostasis?

A

antagonistic regulation

94
Q

what are the 3 divisions of the nervous system?

A

-sympathetic
-parasympathetic
-enteric

95
Q

where does brain control of the autonomic NS come from?

A

hypothalamus
reticular formation (RF)

96
Q

what is the common order of the structures in the autonomic NS?

A

spinal cord -> preganglionic neuron -> ganglion -> postsynaptic neuron -> effector

97
Q

where are the ganglia in the sympathetic NS vs the parasympathetic NS?

A

Symp: near the spinal cord
Parasymp: near the effector

98
Q

what are differences in the size of the dendritic trees and their neural inputs between the sympathetic and pararsympathetic NS?

A

symp: large dendritic trees, many neural inputs
parasymp: few dendrites, fewer neural inputs

99
Q

does the sympathetic or parasympathetic NS have a long preganglionic neuron and a short postganglionic neuron?

A

parasympathetic
-sympathetic has short pregang and long postgang

100
Q

what type of outflow does the sympathetic NS have and what does that mean?

A

thoracolumbar outflow
-neurons come from the thorastic and lumbar region of the spinal cord

101
Q

where do the preganglionic neurons come from?

A

lateral horns of the spinal cord

102
Q

what type of activation does the homeostatic activity have?

A

tonic activation (persistent activity)
-discrete (not none-or-all)
-short lasting effects

103
Q

what type of activation does the fight/flight activity have in the sympathetic NS?

A

diffuse activation
-all activate strongly at the same time very quickly
-long lasting

104
Q

what type of outflow does the parasympathetic NS have and what does that mean?

A

craniosacral outflow
-has cranial nerves from the brainstem
-has sacral spinal cord nerves from the lateral horns

105
Q

what type of activation does the parasympathetic NS have?

A

discrete, tonic activation
-short lasting effects

106
Q

what does the preganglionic neuron do?

A

release ACh
-has both types of ACh-R (nicotinic and muscarinic)

107
Q

what does the neuroeffector synapse do?

A

-has axonal varicostities
-released the NT from postganglionic neuron
-the NT travels long distances

108
Q

what does the postganglionic neuron do?

A

it has different NT at effectors

109
Q

what NT is used in the parasympathetic NS?

A

ACh
-uses mainly muscarinic receptors (M1 & M2)
-found in GI tract and cardio system
-controls K+, Ca2+, and (NO) synthesis

110
Q

what NT is used in the sympathetic NS?

A

NE
-uses both beta and alpha receptor subtypes

111
Q

what NT is used in the Enteric NS?

A

ACh and NE
-uses a neuropeptide as a co-transmitter

112
Q

what do the adrenal glands do and what is special about their neurons?

A

-takes ACh and turns it into NE to be released into the blood
-maintains sympathetic NS
-responsible for long lasting effects in emergencies
-only has ONE neuron

113
Q

HEART: does in increase or decrease in sympathetic and parasympathetic NS

A

sym: increase
parasym: decrease

114
Q

RESPIRATION: does in increase or decrease in sympathetic and parasympathetic NS

A

sym: increase
parasym: decrease

115
Q

SALVATION: does in increase or decrease in sympathetic and parasympathetic NS

A

sym: increase (putrid)
parasym: decrease (profuse)

116
Q

GI: does in increase or decrease in sympathetic and parasympathetic NS

A

sym: decrease
parasym: increase

117
Q

IMMUNE SYSTEM: does in increase or decrease in sympathetic and parasympathetic NS

A

sym: decrease
parasym: increase

118
Q

SWEAT GLANDS: does in increase or decrease in sympathetic and parasympathetic NS

A

sym: increase
parasym: NONE

119
Q

ADRENAL GLANDS: does in increase or decrease in sympathetic and parasympathetic NS

A

sym: increasae
parasym: NONE

120
Q

IRIS: does in increase or decrease in sympathetic and parasympathetic NS

A

sym: increase (radial)
parasym: increase (sphincter)

121
Q

what is conscious arousal?

A

level of alertness and how conscious/aware you are of the things around you
-autonomic inputs

122
Q

what are central sensory afferents? (CSA)

A

sensory info
-external: environment
-internal: somatosensory

123
Q

where sensory afferents send their signal to?

A

-directly to the brain (rapid, point-to-point)
-to the reticular formation (slow, indirect)

124
Q

what is the reticular activating system?

A

gets inputs from the sensory afferents and creates two general cortical arousal streams

125
Q

what are the two streams in the reticular activating system?

A

Ventral Stream: RF –> BF
Dorsal Stream: RF –> Thalamus –> BF

126
Q

what do the NTs (ACh, NE, 5-HT) do to arousal in the reticular formation? where in the brain does the signal come from?

A

ACh = increase arousal (ventral RF)
NE = increase arousal (locus coeruleus)
5-HT = decrease arousal (raphe nuclei)

127
Q

what does ACh and GABA do in the basal forebrain?

A

ACh: increase arousal (inhibited by adenosine, stimulated by histamine)
GABA: modulates arousal (increase in GABA = decrease in arousal, decrease in GABA = increase in arousal)

128
Q

what are the agonists and antagonists in the basal forebrain?

A

agonists: barbiturates, ETOH, benzodiazepines
ANT: picrotoxin, strychnine

129
Q

what is pain and what is its function?

A

-based on individuals perception because it has many components
-subjective response
-signals for potential injury and motivates behavior

130
Q

what is nociception?

A

sensation of stimulus
-detects and transduces pain into a neural signal

131
Q

nociceptor structure and the three types

A

-have free nerve endings (no structures surrounding them)
-no specificity
-types: mechanical, thermal, chemical

132
Q

what are the two branches in the anterolateral system (parallel pain pathways), and what do they detect?

A

Sensory Discriminative Branch: locus of stimulus, intensity, type
Affective Motivational Branch: emotion, behavior

133
Q

where are 1st order sensory neurons located at, where to they project to, and what do they release?

A

-located in the unipolar dorsal root ganglia neuron
-project to gray matter of dorsal horn
-releases glutamate (fast) and substance P (slow & long)

134
Q

where are 2nd order sensory neurons located at and where does it send its signal to?

A

-located at the gray part of the dorsal horn of the spinal cord
-sends signal to the anterolateral columns in two directions

135
Q

where do the two signals in the anterolateral columns go to?

A

-either the brainstem periaqueductal gray (PAG)
-or thalamus -> cortex

136
Q

what is behavioral analgesia?

A

decreased perceived pain w/o loss of consciousness
-stress induced
-decreases nociception and subjective experience
-TEMPORARY

137
Q

what type of receptors does analgesia act on?

A

opioid-mediated receptors (Endorphins)

138
Q

how is naloxone a direct ANT for opioids?

A

high affinity but low efficacy for them (wants to bind them, but produces a small effect)
-insurmountable action

139
Q

what types of things are naloxone sensitive?

A

things that cause analegesia to bind to the opioid receptors
-stress-induced things
-acupuncture
-placebo effect

140
Q

what types of things are naloxone insensitive?

A

hypnosis
meditation

141
Q

what are the two analgesic mechanisms?

A

-opioid-mediated
-NON opioid-mediated

142
Q

where is the opioid-mediated mechanism located at? (2 places)

A

-PAG of the supra-spinal cord (above SC)
-Dorsal horn of the spinal cord

143
Q

what types of things are non opioid-mediated mechanisms?

A

glutamate, estrogen, cholinergic, endocannabinoids, chronic pain

144
Q

what is the descending analgesic circuit pathway?

A

PAG –> activates opioid –> inhibits GABA –> active ACh –> LC –> RN –> spinal cord

145
Q

what types of neurons increase and decrease in the spinal cord of the descending analgesic circuit?

A

-INCREASE of inhibitory neurons (GABA, enkephalin) through excitation (+)
-DECREASE of excitatory neurons through inhibition (-)

Drugs & Behavior (5 decks)

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