Discussion 4

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Physiology of Behavior

Twelfth Edition

Chapter 4

Psychopharmacology

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Principles of Psychopharmacology

Sites of Drug Action

Neurotransmitters and Neuromodulators

Principles of Psychopharmacology

Overview

Pharmacokinetics

Drug Effectiveness

Effects of Repeated Administration

Placebo Effects

Sites of Drug Action

Effects on Production of Neurotransmitters

Effects on Storage and Release of Neurotransmitters

Effects on Receptors

Effects on Reuptake or Destruction of Neurotransmitters

Neurotransmitters and Neuromodulators

Amino acids

Acetylcholine

The Monoamines

Peptides

Lipids

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Learning Objectives (1 of 3)

4.1 Differentiate between the terms drug, drug effect, and site of action.

4.2 Describe how the four steps of pharmacokinetics are related.

4.3 Identify how drug effectiveness can be measured and list two reasons why drugs vary in their effectiveness.

4.4 Differentiate between tolerance, sensitization, and withdrawal effects following repeated use of a drug.

4.5 Describe a placebo and the placebo effect.

Principles of Psychopharmacology

Overview

Pharmacokinetics

Drug Effectiveness

Effects of Repeated Administration

Placebo Effects

Sites of Drug Action

Effects on Production of Neurotransmitters

Effects on Storage and Release of Neurotransmitters

Effects on Receptors

Effects on Reuptake or Destruction of Neurotransmitters

Neurotransmitters and Neuromodulators

Amino acids

Acetylcholine

The Monoamines

Peptides

Lipids

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Learning Objectives (2 of 3)

4.6 Summarize how drug molecules can increase or decrease neurotransmitter synthesis.

4.7 Distinguish between the effects of agonists and antagonists on storage and release of neurotransmitters.

4.8 Contrast the effects of agonists and antagonists at the receptor.

4.9 Describe the effects of agonists on neurotransmitter reuptake and degradation.

4.10 Compare the features of the amino acid neurotransmitter systems.

Principles of Psychopharmacology

Overview

Pharmacokinetics

Drug Effectiveness

Effects of Repeated Administration

Placebo Effects

Sites of Drug Action

Effects on Production of Neurotransmitters

Effects on Storage and Release of Neurotransmitters

Effects on Receptors

Effects on Reuptake or Destruction of Neurotransmitters

Neurotransmitters and Neuromodulators

Amino acids

Acetylcholine

The Monoamines

Peptides

Lipids

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Learning Objectives (3 of 3)

4.11 Summarize the features of the acetylcholine system.

4.12 Summarize the key features of the monoamine systems.

4.13 Contrast the features of peptide neurotransmitters with classical neurotransmitters.

4.14 Summarize the features of the lipid neurotransmitter systems.

Principles of Psychopharmacology

Overview

Pharmacokinetics

Drug Effectiveness

Effects of Repeated Administration

Placebo Effects

Sites of Drug Action

Effects on Production of Neurotransmitters

Effects on Storage and Release of Neurotransmitters

Effects on Receptors

Effects on Reuptake or Destruction of Neurotransmitters

Neurotransmitters and Neuromodulators

Amino acids

Acetylcholine

The Monoamines

Peptides

Lipids

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Principles of Psychopharmacology

What is a drug?

Exogenous chemical

Alters functions of certain cells

Drug effects:

Changes drug produces in an animal’s physiological processes and behavior

Site of action:

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

Pharmacology: the study of the effects of drugs on the nervous system and behavior

Drug: “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.”

Drug effects: changes we can observe in an individual’s physiological processes and behavior

Site of action: 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

Drug Effect

Changes drug produces in an animal’s physiological processes and behavior

Sites of Action

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

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Pharmacokinetics

Movements of drugs, including process by which drugs are:

Absorbed

distributed within the body

Metabolized

excreted

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Figure 4.2 The Four Components of Pharmacokinetics

Figure 4.2 page 92

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Absorption: Routes of Administration (1 of 2)

Intravenous (IV) Injection

Intraperitoneal (IP) Injection

Intramuscular (IM) Injection

Subcutaneous (SC) Injection

Oral Administration

Sublingual Administration

Intrarectal Administration

Intravenous (IV) Injection – injection of a substance directly into a vein.

Intraperitoneal (IP) Injection – injection of a substance into the peritoneal cavity, the space that surrounds the stomach, intestines, liver, and other abdominal organs.

Intramuscular (IM) Injection – injection of a substance into a muscle.

Subcutaneous (SC) Injection – injection of a substance into the space beneath the skin.

Oral Administration – administration of a substance into the mouth so that it is swallowed.

Sublingual Administration – administration of a substance by placing it beneath the tongue.

Intrarectal Administration – administration of a substance into the rectum. Inhalation – administration of a vaporous substance into the lungs.

Topical Administration – administration of a substance directly onto the skin or mucous membrane.

Intracerebral Administration – administration of a substance directly into the brain.

Intracerebroventricular (ICV) Administration – administration of a substance into one of the cerebral ventricles.

Inhalation

Topical Administration

Intracerebral Administration

Intracerebroventricular (ICV) Administration

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Absorption: Routes of Administration (2 of 2)

Inhalation

Topical Administration

Intracerebral Administration

Intracerebroventricular (ICV) Administration

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Figure 4.3 Cocaine in Blood Plasma

The graph shows the concentration of cocaine in blood plasma after intravenous injection, inhalation, oral administration, and sniffing.

Figure 4.3 page 92

.(Adapted from Feldman, R. S., Meyer, J. S., and Quenzer, L. F., Principles of Neuropsychopharmacology, Sunderland, MA: Sinauer Associates, 1997; after Jones, R. T., NIDA Research Monographs, 1990, 99, 30–41.)

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Metabolism and Excretion

Inactivation and excretion

Enzymes deactivate drugs (e.g., liver)

Drugs are eventually excreted (e.g., kidneys)

Drugs do not remain in the body indefinitely.

Many are deactivated by enzymes, and all are eventually excreted, primarily by the kidneys.

The liver plays an especially active role in enzymatic deactivation of drugs, but some deactivating enzymes are also found in the blood.

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Drug Effectiveness

Dose-Response Curve

Graph of magnitude of effect of drug as function of the amount of drug administered

Therapeutic Index

Ratio between dose that produces desired effect in 50% of animals and dose that produces toxic effects in 50% of animals

Affinity

Readiness with which two molecules join together

Why do drugs vary in their effectiveness?

Different site of action, affinity of drug with site of action

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Figure 4.4 A Dose-Response Curve

Increasingly stronger doses of the drug produce increasingly larger effects until the maximum effect is reached. After that point, increments in the dose do not produce any increments in the drug’s effect. However, the risk of adverse side effects increases.

Figure 4.4 page 93

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Figure 4.5 Dose-Response Curves for Morphine

The dose-response curve on the left shows the analgesic effect of morphine, and the curve on the right shows one of the drug’s adverse side effects: its depressant effect on respiration. A drug’s margin of safety is reflected by the difference between the dose-response curve for its therapeutic effects and that for its adverse side effects.

Figure 4.5 page 94

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Effects of Repeated Administration

Tolerance

Sensitization

Withdrawal

Tolerance: Decrease in the effectiveness of a drug that is administered repeatedly

Sensitization: Increase in the effectiveness of a drug that is administered repeatedly

Withdrawal: Appearance of symptoms opposite to those produced by drug when drug is administered repeatedly and then suddenly no longer taken

Physical dependence

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Placebo Effects

Placebo

inactive substance

External factors

Expectations

Used as control group in research

Placebo responses can be the result of changes in motivation, expectation, or forms of learning such as classical conditioning (Price et al., 2008)

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Sites of Drug Action

Agonist

facilitate postsynaptic effects

Antagonist

block or inhibit postsynaptic effects

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Effects on Production of Neurotransmitters

Neurotransmitters synthesized by presynaptic neurons

Some drugs act as precursors e.g. L-DOPA

Some drugs deactivate enzymes e.g. PCPA

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Effects on Storage and Release of Neurotransmitters

Neurotransmitters stored in synaptic vesicles

Vesicle transporters

Some drugs block vesicle transporters, e.g. reserpine

Neurotransmitter release at terminal button

Some drugs prevent release here, e.g. botulism toxin

Some drugs trigger release of neurotransmitter, e.g. alcohol

Vesicle transporters pump molecules of the neurotransmitter across the vesicle membrane to fill the vesicles

Drugs that block vesicle transporters act as antagonists e.g. reserpine blocks for monoamine transporter

Drugs that prevent release at terminal button are also antagonists, e.g. botox prevents release of acetylecholine

Drugs that trigger release at terminal button are agonists, alcohol is agonist for GABA

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Figure 4.7 Drug Effects on Synaptic Transmission

Figure 4.7 page 98

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Effects on Postsynaptic Receptors

Direct agonist

Receptor blocker

Noncompetitive binding

Direct Agonist

Drug that binds with and activates receptor

Receptor Blocker

Drug that binds with receptor but does not activate it; prevents natural ligand from binding with receptor

Direct antagonist

Noncompetitive Binding

Binding of a drug to a site on a receptor; does not interfere with the binding site for the principal ligand

Indirect antagonist

E.g. PCP and ketamine

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Figure 4.8 Drug Actions at Binding Sites

(a) Competitive binding: Direct agonists and antagonists act directly on the neurotransmitter binding site.

(b) Noncompetitive binding: Indirect agonists and antagonists act on an alternative binding site and modify the effects of the neurotransmitter on opening of the ion channel.

Figure 4.8 page 99

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Effects on Reuptake or Destruction of Neurotransmitters

Molecules of neurotransmitter

Drugs can interfere with processes

Drugs can interfere with either of these processes. In the first case, molecules of the drug attach to the transporter molecules responsible for reuptake and inactivate them, thus blocking reuptake

In the second case, molecules of the drug bind with the enzyme that normally destroys the neurotransmitter and prevents the enzymes from working

Molecules of neurotransmitter

taken back into terminal button through process of reuptake

or they are destroyed by an enzyme

Drugs can interfere with processes

blocking reuptake

binding and preventing enzyme from working

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Neurotransmitter and Neuromodulators: Amino Acids (1 of 2)

Glutamate: the main excitatory neurotransmitter in the brain

NMDA receptor

AMPA receptor

Kainate (kay in ate) receptor

Metabotropic (meh tab a troh pik) glutamate receptor

NMDA Receptor

a specialized ionotropic glutamate receptor; controls a calcium channel that is normally blocked by Mg2+ ions; has several other binding sites

AMPA Receptor

an ionotropic glutamate receptor that controls a sodium channel; stimulated by AMPA

Kainate Receptor (kay in ate)

an ionotropic glutamate receptor that controls a sodium channel; stimulated by kainic acid

Metabotropic Glutamate Receptor (meh tab a troh pik)

a category of metabotropic receptors that are sensitive to glutamate

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Neurotransmitter and Neuromodulators: Amino Acids (2 of 2)

GABA: the main inhibitory neurotransmitter in the brain; produced from glutamic acid by the action of an enzyme called GAD

Benzodiazepine (ben zoe dy azz a peen)

Anxiolytic (angz ee oh lit ik)

Allylglycine

Muscimol

Bicuculline

Allylglycine – a drug that inhibits the activity of GAD and thus blocks the synthesis of GABA

Muscimol – a direct agonist for the GABA binding site on the GABAA receptor

Bicuculline – a direct antagonist for the GABA binding site on the GABAA receptor

Benzodiazepine – a category of anxiolytic drugs; and indirect agonist for the GABAA receptor

Anxiolytic – an anxiety-reducing effect

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Table 4.1 Neurotransmitter Systems (1 of 2)

Neurotransmitter	Examples of CNS Functions	Examples of PNS Functions
Glutamate	Excitatory; interacts with other neurotransmitter systems	N/A
GABA	Inhibitory, interacts with other neurotransmitter systems	N/A
Acetylcholine (ACh)	Learning, memory, REM sleep	Muscle contraction
Dopamine	Voluntary movement, attention, learning, reinforcement, planning, Problem solving	N/A

Table 4.1 page 101

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Table 4.1 Neurotransmitter Systems (2 of 2)

Neurotransmitter	Examples of CNS Functions	Examples of PNS Functions
Norepinephrine/Epinephrine	Vigilance	Autonomic nervous system regulation (regulate heart rate ,blood pressure, etc.
Serotonin	Mood regulation, eating, sleep, dreaming, arousal, impulse control	Invoked in the enteric nervous system (digestive tract)
Histamine	Wakefulness	Immune response
Opioids	Reinforcement, pain modulation	Pain modulation
Endocannabinoids	Appetite regulation	Immune response

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Figure 4.9 NMDA Receptor

This schematic illustration of an NMDA receptor shows its binding sites. Amino Acids: Glutamate

Figure 4.9 page 102

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Figure 4.10 GABA Receptor

This schematic illustration of a GABAA receptor shows its binding sites.

Figure 4.10 page 103

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Neurotransmitter and Neuromodulators: Acetylcholine

Primary neurotransmitter secreted by efferent axons of the PNS

Major concentrations of ACh in the CNS include:

Dorsolateral Pons (role in REM sleep)

Basal Forebrain (role in learning)

Medial Septum (role in memory)

Acetylcholine is the primary neurotransmitter secreted by efferent axons of the peripheral nervous system.

All muscular movement is accomplished by the release of acetylcholine, and ACh is also found in the ganglia of the autonomic nervous system and at the target organs of the parasympathetic branch of the ANS.

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Table 4.2 Drugs that Act on the Glutamate and GABA Systems

Drug	Mechanism	Effect
Glutamate	No data	No data
PCP	Indiect NMDA receptor antagonist	Impairs learning
AP5	NMDA receptor antagonist	Impairs learning
NMDA	NMDA receptor agonist	Used in research to study this receptor
AMPA	AMPA receptor agonist	Used in research to study this receptor
Kainate	Kainate receptor agonist	Used h research to study this receptor
GABA	No data	No data
Allylgtycine	Inhibits GABA synthesis	Seizures
Muscimol	GABA receptor agonist	Sedation
Bicueufine	GABA receptor antagonist	Seizures
Benzodiazepines	Indirect GAGA receptor agonists	Anxiolytic, sedation, memory impairment, muscle relaxation
Barbiturates	Indirect GAGA receptor agonists	Sedation, memory impairment, muscle relaxation
Alcohol	Indirect GABA receptor agonist (among other mechanisms)	Sedation, memory impairment, muscle relaxation

Table 4.2 page 104

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Figure 4.11 Acetylcholinergic Pathways in a Rat Brain

This schematic figure shows the locations of the most important groups of acetylcholinergic neurons and the distribution of their axons and terminal buttons.

Figure 4.11 page 104

(Adapted from Woolf, N. J., Cholinergic systems in mammalian brain and spinal cord, Progress in Neurobiology, 1991, 37, 475–524.)

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Figure 4.12 Synthesis of Acetylcholine

Figure 4.12 and 4.13 page 1.5

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Figure 4.13 Destruction of Acetylcholine by Acetylcholinesterase

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Table 4.3 Drugs that Act on the Acetylcholine System

Drug	Mechanism	Effect
Botulinum toxin	Prevents release of ACh in PNS	Prevents muscle contraction
Black widow spider venom	Stimulates release of ACh in PNS	Stimulates muscle contraction
Neostigmine	Inhibits AChE	Increases effect of ACh at receptors; used to treat symptoms of myasthenia gravis
Nicotine	Agonist at ionotropic receptors	Increases attention, reinforcing effects
Muscarine	Agonist at metabotropic receptors	Toxic, hallucinogenic effects
Curare	Antagonist at ionotropic receptors	Prevents muscle contraction
Atropine	Antagonist at metabotropic receptors	Blocks pupil constriction, saliva production

Table 4.3 page 106

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The Monoamines

Dopamine (DA) (dope a meen)

Neurotransmitter

one of the catecholamines

L-DOPA (ell dope a)

Levorotatory form of DOPA

the precursor of the catecholamines

often used to treat Parkinson’s disease because of its effect as a dopamine agonist

Norepinephrine (NE) (nor epp i neff rin)

Epinephrine (epp i neff rin)

Dopamine

A catecholamine synthesized from L-DOPA.

Major CNS dopaminergic systems include:

Nigrostriatal System (role in movement)

Mesolimbic System (role in reinforcement/reward)

Mesocortical System (role in short-term memory, planning, and problem solving)

Norepinephrine (NE) (nor epp i neff rin)

one of the catecholamines; a neurotransmitter found in the brain and in the sympathetic division of the autonomic nervous system

Epinephrine (epp i neff rin)

one of the catecholamines; a hormone secreted by the adrenal medulla; serves also as a neurotransmitter in the brain

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Table 4.4 Classification of the Monoamine Neurotransmitters

Catecholamines	Indolamine	Ethylamine
Dopamine	Secotorin	Histamine
Norepinephrine	No data	No data
Epinephrine	No data	No data

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Dopamine

Catecholamine synthesized from L-DOPA

Major CNS dopaminergic systems include:

Nigrostriatal (nigh grow stry ay tul) system

Mesolimbic (mee zo lim bik) system

Mesocortical (mee zo kor ti kul) system

Parkinson’s Disease:

Neurological disease

Characterized by tremors, rigidity of limbs, poor balance, and difficulty in initiating movements

Caused by degeneration of nigrostriatal system

Nigrostriatal System (nigh grow stry ay tul)

System of neurons originating in substantia nigra and terminating in neostriatum (caudate nucleus and putamen)

Mesolimbic System (mee zo lim bik)

System of dopaminergic neurons originating in ventral tegmental area and terminating in nucleus accumbens, amygdala, and hippocampus

Mesocortical System (mee zo kor ti kul)

System of dopaminergic neurons originating in ventral tegmental area and terminating in prefrontal cortex(nigh grow stry ay tul)

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Figure 4.14 Dopaminergic Pathways in a Rat Brain

This schematic figure shows the locations of the most important groups of dopaminergic neurons and the distribution of their axons and terminal buttons.(Adapted from Fuxe, K., Agnati, L. F., Kalia, M., et al., Dopaminergic systems in the brain and pituitary, in Basic and Clinical Aspects of Neuroscience: The Dopaminergic System,edited by E. Fluckinger, E. E. Muller, and M. O. Thomas,Berlin: Springer–Verlag, 1985.)

Figure 4.14 page 107

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Figure 4.16 Effects of Low and High Doses of Apomorphine

At low doses, apomorphine serves as a dopamine antagonist; at high doses, it serves as an agonist.

Figure 4.16 page 109

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Figure 4.17 Role of Monoamine Oxidase

This schematic shows the role of monoamine oxidase in dopaminergic terminal buttons and the action of deprenyl.

Figure 4.17 page 109

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Norepinephrine

Norepinephrine: found in the brain and in the sympathetic division of the autonomic nervous system

Moclobemide

Locus Coeruleus

Axonal Varicosities

Receptors subtypes

Moclobemide – a drug that blocks the activity of MAO-A; acts as a noradrenergic agonist

Locus Coeruleus – a dark-colored group of noradrenergic cell bodies located in the pons near the rostral end of the floor of the fourth ventricle

Axonal Varicosities – an enlarged region along the length of an axon that contains synaptic vesicles and releases a neurotransmitter or neuromodulator. Most norepinephrine is released in this way

Idazoxan – a drug that blocks presynaptic noradrenergic 2 receptors. Facilitates the synthesis and release of NE

Several receptor subtypes exist: four types, α1- and α2-adrenergic receptors and β1- and β2-adrenergic receptors, that are sensitive to both norepinephrine and epinephrine

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Figure 4.18 Noradrenergic Pathways in a Rat Brain

This schematic figure shows the locations of the most important groups of noradrenergic neurons and the distribution of their axons and terminal buttons. (Adapted from Cotman, C. W. and McGaugh, J. L., Behavioral Neuroscience: An Introduction, New York: Academic Press, 1980.)

Figure 4.18 page 110

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Serotonin

Serotonin (5-HT) (sair a toe nin): Indolamine neurotransmitter; also called 5-hydroxytryptamine

Plays a role in the regulation of mood, control of eating, sleep, and arousal and in the regulation of pain

Serotonergic neurons are involved somehow in the control of dreaming

PCPA

Fluoxetine (Prozac)

Fenfluramine

MDMA

Fluoxetine (Prozac) – a drug that inhibits the reuptake of 5-HT

Fenfluramine – a drug that stimulates the release of 5-HT

MDMA – a drug that serves as a noradrenergic and serotonergic agonist, also known as “ecstasy”; has excitatory and hallucinogenic effects

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Figure 4.19 Serotonergic Pathways in a Rat Brain

This schematic figure shows the locations of the most important groups of serotonergic neurons and the distribution of their axons and terminal buttons

Figure 4.19 page 111

.(Adapted from Consolazione, A. and Cuello, A. C., CNS serotonin pathways, pp. 29—61, in Biology of Serotonergic Transmission, edited by N. N. Osborne, Chichester: England: Wiley & Sons, 1982.)

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Histamine

Cell bodies found in tuberomammillary nucleus of posterior hypothalamus

Send axons to widespread regions of cerebral cortex and brain stem. Histamine plays an important role in wakefulness.

Histamine:

Produced from amino acid, histidine, by the action of enzyme histidine decarboxylase

The cell bodies of histaminergic neurons are found in only one place in the brain: the tuberomammillary nucleus, located in the posterior hypothalamus.

Histaminergic neurons send their axons to widespread regions of the cerebral cortex and brain stem. Histamine plays an important role in wakefulness.

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Figure 4.21 Histaminergic Pathways in a Rat Brain

This schematic shows the locations of the most important group of histaminergic neurons and the distribution of their axons and terminal buttons.

Figure 4.21 page 112

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Table 4.5 Drugs that Act on Monoamine Systems (1 of 2)

Drug	Mechanism	Effect
Dopamine	No data	No data
i -Dope	DA precursor	Enhances DA effects; treats Parkinson's disease symptoms
AM PT	Blocks tyrosine hydroxylase	Used in research
Apomorphine	D2 antagonist	Used in research
Methylphenidate	Blocks DA reuptake	Stimulant: used to treat symptoms of ADHD
Cocaine	Blocks DA reuptake	Stimulant and reinforcing effects
Chlorpromazine	D2 receptor antagonist	Used to treat positive symptoms of schizophrenia
Norepinephrine	No data	No data
Idazoxan	0, autoreceptor antagonist	Used in research, may have antidepressant effects

Table 4.5 page 113

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Table 4.5 Drugs that Act on Monoamine Systems (2 of 2)

Drug	Mechanism	Effect
Serotonin	No data	No data
PCPA	Blocks tryptophan hydroxylase	Used in research
Fluoxetine	Blocks 5-HT reuptake	Used to treat symptoms of depression
Fenfluramine	Blocks 5-HT reuptake, causes 5-HT release	Appetite suppressant, no longer prescribed
MDMA	Blocks 5-1-IT reuptake, causes 5-1-IT release	Drug of abuse
Histamine	No data	No data
Diphenhydramine	Blocks histamine receptors	Sedation
Multiple Systems	No data	No data
Reserpine	Blocks monoamine storage in vesicles	Sedation, depression
AMPT	Blocks tyrosine hydroxylase	Used in research
Moclobemide	MAO inhibitor	Used to treat symptoms of depression
Deprenyl	MAO inhibitor	Used to treat Parkinson's disease

Table 4.5 page 113

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Neurotransmitter and Neuromodulators: Peptides and Lipids

Peptides:

Two or more amino acids linked with peptide bond

Endogenous opioids

Lipids:

Best known example is endocannibinoids

Peptides are released from all parts of terminal button

Endocannibinoid: anandamide

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Table 4.6 Drugs that Act on Peptide and Lipid Neurotransmitter Systems

Drug Peptides	Mechanism	Effect
Opiates	Opioid receptor agonists	Analgesia, sedation, reinforcing
Naloxone	Opioid antagonist	Reverses opioid overdose
Lipids	No data	No data
TEC	Cannabinoid receptor agonist	Increases appetite produces analgesia, cognitive it effects
Rimonabant	Cannabinoid receptor antagonist	Suppresses appetite, used in smoking cessation
MAFP	Inhibits FAAH	Used in research. Increases Cannabinoid system activity
AM 1172	Blocks cannabinoid reuptake	Used in research. Increases Cannabinoid system activity

Discussion 4

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