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Physiology of Behaviour > Chapter 4: Psychopharmacology > Flashcards

Chapter 4: Psychopharmacology Flashcards

1
Q

Study of the effects of drugs on the nervous system and behavior.

A

Psychopharmacology

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2
Q

An exogenous chemical not necessary for normal cellular functioning that significantly alters the functions of certain cells of the body when taken in relatively low doses.

A

Drug

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3
Q

The changes we can observe in an individual’s physiological processes and behavior.

A

Drug effects

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4
Q

The points at which molecules of drugs interact with molecules located on or in cells of the body, thus affecting some biochemical processes of these cells.

A

Sites of action

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5
Q

Study of all drugs.

A

Pharmacology

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6
Q

Examples of drug abuse.

A

Heroin
Cocaine

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7
Q

Examples of therapeutic drugs.

A

Antidepressants
Antipsychotics

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8
Q

Includes the steps by which drugs are (1)
absorbed, (2) distributed within the body, (3) metabolized, and (4) excreted.

A

Pharmacokinetics

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9
Q

4 steps involved in pharmacokinetics.

A

Absorption
Distribution
Metabolism
Excretion

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10
Q

Injection into a vein; fastest route.

A

Intravenous (IV) injection

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11
Q

Drug is injected through the abdominal wall into the peritoneal cavity; rapid but not as rapid as an IV injection.

A

Intraperitoneal (IP) injection

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12
Q

The space that surrounds the stomach, intestines, liver, and other abdominal
organs.

A

Peritoneal cavity

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13
Q

Made directly into a large muscle, such as those found in the upper arm, thigh, or buttocks; drug is absorbed into the bloodstream through the capillaries that supply the muscle.

A

Intramuscular (IM) injection

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14
Q

Drug is injected into the space beneath the skin.

A

Subcutaneous (SC) injection

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15
Q

Most common form of administering therapeutic drugs to humans.

A

Oral administration

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16
Q

Accomplished by placing drugs beneath the tongue; drug is absorbed into the bloodstream by the capillaries that supply the mucous membrane that lines the mouth.

A

Sublingual administration

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17
Q

Drugs are inhaled through the route from the lungs; has very rapid effects.

A

Inhalation

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18
Q

Drugs are absorbed directly through the skin.

A

Topical administration

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19
Q

Drugs are sniffed; drugs enter circulation through the mucous membrane of the nasal passages.

A

Insufflation

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20
Q

Drugs are injected directly to the brain.

A

Intracerebral administration

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21
Q

Drug is injected to the cerebral ventricle.

A

Intracerebroventricular (IVC) administration

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22
Q

Drug is administered and absorbed through tissues.

A

Absorption

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23
Q

Drug is distributed throughout the body and blood.

A

Distribution

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24
Q

Drug is changed to an inactive form by enzymes (usually in liver).

A

Metabolism

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25
Q

Drug is excreted in urine by kidneys.

A

Excretion

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26
Q

The ability of fat-based molecules to pass through cell membranes.

A

Lipid solubility

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27
Q

Best way to measure the effectiveness of a drug by plotting effects of the drug on the vertical axis and dose of the drug on the horizontal axis.

A

Dose-response curve

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28
Q

One measure of a drug’s margin of safety; obtained by administering varying doses of the drug to a group of laboratory animals or human
volunteers.

A

Therapeutic index

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29
Q

2 reasons drugs vary in their effectiveness.

A

Sites of action
Affinity/ Affinity of the drug with its site of action

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30
Q

The readiness with which the two molecules
join together.

A

Affinity

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31
Q

Effects will diminish when a drug is administered repeatedly.

A

Tolerance

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32
Q

Repeated doses of a drug produce greater and greater effects; opposite of tolerance.

A

Sensitization

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33
Q

The opposite of the effects of the drug itself.

A

Withdrawal symptoms

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34
Q

When a person has repeatedly used a drug enough to produce withdrawal symptoms when they stop using it.

A

Physical dependence

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35
Q

Involves a decrease in the effectiveness of binding with receptors; receptors become less sensitive to the drug and their affinity for the drug decreases, or the receptors decrease in number.

A

First compensatory mechanism

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36
Q

Involves the process that couples the receptors to
ion channels in the membrane or to the production of second messengers; After prolonged stimulation of the receptors, one or more steps in the coupling process become less effective.

A

Second compensatory mechanism

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37
Q

An inactive substance that can produce a physiological or psychological effect.

A

Placebo

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38
Q

The points at which molecules of drugs
interact with molecules located on or in cells of the body.

A

Sites of action

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39
Q

Drugs that block or inhibit the postsynaptic effects.

A

Antagonists

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40
Q

Drugs that facilitate postsynaptic effects.

A

Agonists

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41
Q

Drugs that are considered agonists because administering them increases activity of the neurotransmitter system.

A

Precursor drugs

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42
Q

Pump molecules of the neurotransmitter across the vesicle membrane, filling the vesicles.

A

Vesicle transporters

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43
Q

An example of a drug that blocks vesicle transporters for monoamine neurotransmitter systems.

A

Reserpine

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44
Q

The neurotransmitter responsible for signaling muscle contractions in the PNS

A

Acetylcholine

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45
Q

A drug that mimics the effects of a neurotransmitter.

A

Direct agonist

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46
Q

Drugs that prevent the neurotransmitter from activating the receptor.

A

Receptor blocker/ Direct antagonists

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47
Q

Binding of a molecule with one of the alternative sites; molecule does not compete with molecules of the neurotransmitter for the same binding site.

A

Noncompetitive binding

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48
Q

Drug attaches to one of these alternative sites and prevents the ion channel from opening.

A

Indirect antagonist

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49
Q

Drug attaches to one of the alternative sites and facilitates the opening of the ion channel.

A

Indirect agonist

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50
Q

Used to treat the symptoms of anxiety; an indirect agonist and requires concurrent binding of GABA to produce its antianxiety effects.

A

Diazepam (Valium)

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51
Q

Used for protein synthesis by all cells of the brain.

A

Amino acids

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52
Q

The main excitatory neurotransmitter in the brain and spinal cord.

A

Glutamate

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53
Q

Package glutamate into vesicles.

A

Vesicle glutamate transporters

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54
Q

4 major types of glutamate receptors.

A

NMDA receptor
AMPA receptor
Kainate receptor
Metabotropic glutamate receptor

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55
Q

The most common glutamate receptor; controls a sodium channel, so when glutamate attaches to the binding site, it produces EPSPs.

A

AMPA receptor

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56
Q

Has similar effects with AMPA receptor.

A

Kainate receptor

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57
Q

Contains at least 6 different binding sites:4 located on the exterior of the receptor and 2 located deep within the ion channel; when open, the ion channel controlled by this receptor permits both sodium and calcium ions to enter the cell.

A

NMDA receptor

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58
Q

2 amino acid neurotransmitters.

A

Glutamate
GABA (gamma-aminobutyric acid)

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59
Q

Amino acid with inhibitory effects.

A

GABA (gamma-aminobutyric acid)

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60
Q

Secondary inhibitory amino acid neurotransmitter.

A

Glycine

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61
Q

Blocks the glutamate binding site on the NMDA receptor and impairs synaptic plasticity and certain forms of learning.

A

AP5 (2-amino-5-phosphonopentanoate)

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62
Q

Serves as an indirect antagonist; when it attaches to its binding site, calcium ions cannot pass through the ion channel.

A

PCP (phencyclidine)

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63
Q

Has similar effects and is thought to bind to the same site as PCP.

A

Ketamine

64
Q

Removes glutamate from the synapse.

A

Excitatory amino acid transporters

65
Q

Breaks down glutamate into its building block precursor (glutamine).

A

Glutamine synthase

66
Q

Produced when there’s too much glutamate stimulation in the synapse; damage neurons by prolonged over excitation.

A

Glutamate excitotoxicity

67
Q

Inactivates GAD and thus prevents the synthesis of GABA.

A

Allylglycine

68
Q

Package GABA into vesicles.

A

Vesicle GABA transporter

69
Q

Serves as a direct agonist for the primary
binding site for GABA.

A

Muscimol

70
Q

Blocks the GABA binding site, serving as a direct antagonist.

A

Bicuculline

71
Q

Drugs include diazepam (Valium) and alprazolam (Xanax), which are used to reduce symptoms of anxiety, reduce seizure activity, and produce muscle relaxation.

A

Benzodiazepines

72
Q

“Anxiety-dissolving” drugs.

A

Anxiolytics

73
Q

Drugs that are related to the benzodiazepines that are effective sleep medications.

A

Zolpidem (Ambien)
Eszopiclone (Lunesta)

74
Q

Inhibits the activity of the GABAA receptor,
thus serving as an indirect antagonist; high enough doses, this drug causes seizures.

A

Picrotoxin

75
Q

Removes GABA from the synapse.

A

GABA transporters

76
Q

A GABA transporter antagonist used to increase availability of GABA and reduce the likelihood of seizures.

A

Tiagabine (Gabitril)

77
Q

Enzyme that breaks down GABA.

A

GABA aminotransferase

78
Q

Blocks the activity of GABA aminotransferase to
increase the amount of GABA available in the synapse.

A

Vigabatrin (Sabril)

79
Q

3 pathways of acetylcholine-releasing neurons that received the most attention from neuroscientists.

A

Those originating in:

Dorsolateral pons
Basal forebrain
Medial septum

80
Q

Acetylcholinergic neurons located in this pathway play a role in REM sleep.

A

Dorsolateral pons

81
Q

The phase of sleep during which dreaming occurs.

A

REM

82
Q

Acetylcholinergic neurons located in this pathway are involved in activating the cerebral cortex and facilitating learning, especially perceptual
learning.

A

Basal forebrain

83
Q

Acetylcholinergic neurons located in this pathway control the electrical rhythms of the hippocampus and modulate its functions, which include the formation of particular kinds of memories.

A

Medial septum

84
Q

The primary neurotransmitter secreted by axons of the PNS that terminate at muscle cells to control muscle contraction.

A

Acetylcholine (ACh)

85
Q

2 precursors of ACh.

A

Choline
Acetyl coenzyme A

86
Q

Required to produce ACh from the precursors.

A

Choline Acetyltransferase (ChAT)

87
Q

Loads ACh into vesicles.

A

Vesicle ACh transporter

88
Q

Produced by Clostridium botulinum; prevents the release of ACh; an extremely potent poison because the paralysis it can cause leads to suffocation.

A

Botulinum toxin (Botox)

89
Q

A bacterium that can grow in improperly canned
food.

A

Clostridium botulinum

90
Q

Stimulates the release of ACh; much less toxic than botulinum toxin.

A

Black widow spider venom

91
Q

2 types of ACh receptors.

A

Nicotinic receptors (ionotropic)
Muscarinic receptors (metabotropic)

92
Q

Stimulates the ionotropic ACh receptor; a drug found in tobacco leaves.

A

Nicotine

93
Q

Stimulates the metabotropic ACh receptor; a drug found in the poison mushroom Amanita muscaria.

A

Muscarine

94
Q

Drug that blocks muscarinic receptors.

A

Atropine

95
Q

Drug that blocks nicotinic receptors.

A

Curare

96
Q

Used to treat symptoms of a hereditary disorder called myasthenia gravis.

A

AChE inhibitors

97
Q

Caused by a person’s immune system
attacking ACh receptors located on skeletal muscles.

A

Myasthenia gravis

98
Q

If given to a person, they will regain some strength because the ACh that is released
has a more prolonged effect on the remaining receptors.

A

Neostigmine

99
Q

A research drug that blocks the choline transporter; reduces the rate of ACh production.

A

Hemicholinium-3

100
Q

Considered “classical” neurotransmitters which involves dopamine, norepinephrine, epinephrine, serotonin, and histamine.

A

Monoamine

101
Q

A family of relatively small molecules that includes the monoamines and ACh.

A

Classical neurotransmitters

102
Q

A subclass of monoamines where the first three neurotransmitters—dopamine, norepinephrine, and epinephrine—belong.

A

Catecholamines

103
Q

Catecholamine which produces both excitatory and inhibitory postsynaptic potentials, depending on the postsynaptic receptor.

A

Dopamine

104
Q

The cell bodies of neurons of this system are located in the substantia nigra and project their axons to the neostriatum: the caudate nucleus and the putamen.

A

Nigrostriatal system

105
Q

An important part of the basal ganglia, which is involved in the control of movement.

A

Neostriatum

106
Q

The cell bodies of neurons of this system are located in the ventral tegmental area and project their axons to several parts of the limbic system, including the nucleus accumbens, amygdala,
and hippocampus.

A

Mesolimbic system

107
Q

The cell bodies of neurons of this system are also located in the ventral tegmental area; their axons project to the prefrontal cortex.

A

Mesocortical system

108
Q

A movement disorder characterized by tremors, rigidity of the limbs, poor balance, and difficulty in initiating movements.

A

Parkinson’s disease

109
Q

The precursor for the two major catecholamine neurotransmitters (dopamine and norepinephrine); an essential amino acid that we must obtain from our diet.

A

Tyrosine

110
Q

Converts dopamine to norepinephrine.

A

Dopamine β-hydroxylase

111
Q

Inactivates tyrosine hydroxylase; serves
as a catecholamine antagonist.

A

AMPT (or α-methyl-p-tyrosine)

112
Q

Prevents the storage of monoamines in synaptic vesicles by blocking the vesicle monoamine transporters.

A

Reserpine

113
Q

Block D2 receptors; alleviate
some symptoms, such as hallucinations.

A

Chlorpromazine

114
Q

A D2 agonist, but it seems to have a greater affinity for presynaptic D2 receptors than for postsynaptic D2 receptors.

A

Apomorphine

115
Q

They result in the release of both dopamine and norepinephrine by causing the transporters for these neurotransmitters to run in reverse, propelling dopamine and norepinephrine into
the synaptic cleft.

A

Amphetamine
Methamphetamine

116
Q

Best known drugs that inhibit the reuptake of dopamine.

A

Amphetamine
Methamphetamine
Cocaine
Methylphenidate (Ritalin)

117
Q

Drugs that simply block dopamine reuptake.

A

Cocaine
Methylphenidate

118
Q

Blocks voltage-dependent sodium channels; sometimes used as a topical anesthetic, especially in the form of eye drops for eye surgery.

A

Cocaine

119
Q

Used to enhance attention and impulse control in attention-deficit/hyperactivity disorder (ADHD).

A

Methylphenidate

120
Q

Regulates the destruction of catecholamines.

A

Monoamine oxidase (MAO)

121
Q

A drug that inhibits the particular form of monoamine oxidase (MAO-B) that is found in dopaminergic terminal buttons.

A

Deprenyl

122
Q

Catecholamine that is found in both the CNS and PNS.

A

Norepinephrine (NE)

123
Q

A nucleus located in the dorsal pons.

A

Locus coeruleus

124
Q

Inhibits the activity of dopamine β-hydroxylase and thus blocks the production of norepinephrine without affecting the production of dopamine; sometimes used by researchers who want to
investigate the norepinephrine system while leaving the dopamine system unaffected.

A

Fusaric acid

125
Q

Beadlike swellings of the axonal branches.

A

Axonal varicosities

126
Q

4 types of adrenergic receptors.

A

α1- and α2-adrenergic receptors
β1- and β2-adrenergic receptors

127
Q

Research drug that blocks α2 autoreceptors and hence acts as an agonist; used to study the actions of the norepinephrine system.

A

Idazoxan

128
Q

Blocks the adrenergic autoreceptor, resulting in symptoms of anxiety and increased heart rate and blood pressure.

A

Yohimbine

129
Q

Acts as an agonist at the norepinephrine autoreceptor, decreasing the activity of this system and reducing heart rate and blood pressure.

A

Clonidine (Catapres)

130
Q

Responsible for removing excess norepinephrine
from the synapse.

A

Norepinephrine transporter

131
Q

The third monoamine neurotransmitter which plays a role in the regulation of mood; in the control of eating, sleep, and arousal; and in the
regulation of pain.

A

Serotonin

132
Q

Amino acid that is the precursor for serotonin.

A

Tryptophan

133
Q

Blocks the activity of tryptophan hydroxylase and thus serves as a serotonergic antagonist.

A

PCPA (p-chlorophenylalanine)

134
Q

Antagonist that is useful in reducing the side effects of chemotherapy and radiation for the treatment of cancer.

A

Ondansetron

135
Q

Partial agonist that is used to treat symptoms of anxiety and depression.

A

Buspirone (­BuSpar)

136
Q

A direct agonist for postsynaptic 5-HT2A receptors in the forebrain; produces distortions of visual perceptions.

A

LSD (lysergic acid diethylamide)

137
Q

Responsible for removing 5-HT from the synapse.

A

Serotonin transporter

138
Q

Used to treat depression, some forms of anxiety disorders, and obsessive-compulsive disorder.

A

Fluoxetine (Prozac)

139
Q

Causes the release of serotonin as well as inhibits its reuptake; was formerly used as an appetite suppressant in the treatment of obesity.

A

Fenfluramine

140
Q

Binds with norepinephrine and 5-HT transporters and causes them to run backward, releasing these neurotransmitters and inhibiting their reuptake, resulting in excitatory and hallucinogenic effects.

A

MDMA
(methylenedioxymethamphetamine or ecstasy)

141
Q

Where the cell bodies of histaminergic neurons are found; located in the posterior hypothalamus.

A

Tuberomammillary nucleus

142
Q

Monoamine neurotransmitter that plays an important role in wakefulness.

A

Histamine

143
Q

Drugs that block histamine receptors.

A

Antihistamines

144
Q

Contained in over-the-counter sleep aids with the
goal of crossing the blood–brain barrier to produce drowsiness.

A

Diphenhydramine

145
Q

Best known families of peptides.

A

Endogenous opioids

146
Q

Example of opiates that reduce pain because they have direct effects on the brain.

A

Opium
Morphine
Heroin
Oxycodone

147
Q

Natural ligands for receptors for opiate drugs.

A

Enkephalins

148
Q

3 different types of opiate receptors.

A

μ (mu)
δ (delta)
Κ (kappa).

149
Q

Opiate receptor antagonists that is used clinically to reverse opiate intoxication or overdose.

A

Naloxone (Narcan)

150
Q

Natural ligands for the receptors that are responsible for the physiological effects of the active ingredient in marijuana.

A

Endocannabinoids

151
Q

The active ingredient of marijuana; stimulates cannabinoid receptors located in specific regions
of the brain.

A

THC (tetrahydrocannabinol)

152
Q

A lipidlike substance; first natural ligand
for the THC receptor.

A

Anandamine

153
Q

2 types of cannabinoid receptors

A

CB1
CB2

154
Q

Drug that block CB1 receptors.

A

Rimonabant

155
Q

A commonly used over-the-counter analgesic that acts on CB1 receptors in the PNS.

A

Acetaminophen (Paracetamol)

156
Q

Deactivates anandamine; present in anandamide-secreting neurons.

A

FAAH (fatty acid amide hydrolase)

157
Q

Inhibits FAAH acting as a cannabinoid agonist.

A

MAFP

Physiology of Behaviour (12 decks)

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