Chapter 4: Psychotropic Drugs

STRUCTURE AND FUNCTION OF THE BRAIN

Functions and Activities of the Brain
Monitor changes us the external world
Monitor the composition of body fluids
Regulate the contractions of skeletal system
Initiate & regulate the basic drives hunger, thirst, sex, aggression self-protection
Mediate conscious sensation
Store & retrieve memories
Regulate mood (affect) & emotions
Think & perform intellectual functions
Regulate the sleep cycle
Produce & interpret language
Process visual & auditory data
Organization of the brain
Brain stem
Vital functions
o Regulation of blood gases & internal organs
o Maintenance of blood pressure
Higher brain activities
o Thought & emotions
Functioning of internal organs
Initial process centre for sensory info which is sent to the cerebral cortex
Regulates entire cycle of sleep & wakefulness & ability of the cerebrum to carry out
conscious mental activity

Cerebellum
Regulation of skeletal muscles coordination & contraction
Maintenance of equilibrium
Cerebrum
Responsible for mental activities & conscious sense of being
Responsible for language & ability to communicate
Cerebral cortex: (outer layer of brain) responsible for conscious sensation & the
initiation of movement
Diff areas:
 o Parietal cortex: touch
o Temporal cortex: sound
o Occipital cortex: vision
The basal ganglia located deep within the grey matter of the cerebrumthey are
involved in the regulation of movement
Other structuresthe amygdala and hippocampus, are involved in emotions, learning,
memory, and basic drives

Visualizing the brain

Neuroimaging techniques
Structural: view changes in brain structure
o computed tomography (CT)
o magnetic resonance imaging (MRI)
Functional: Shows physiological activity in the brain
o positron emission tomography (PET)
use radioactive tag to trace compounds i.e, glucose
In the brain, glucose is related to functional activity in certain areas
untreated schizophrenia, PET scans may show a decreased use of glucose
in the frontal lobes (frontal cortex is associated w/ reasoning)
ppl w/ OCD, increase brain metabolism, in parts of frontal cortex
ppl w/ depression, decrease brain activity in prefrontal cortex
o single-photon emission computed tomography (SPECT

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 The limbic systema group of structures that includes parts of the frontal cortex, the
basal ganglia, and the brain stemis a major area of psychological activity
o The monoamine neurotransmitters (norepinephrine,dopamine, and serotonin)
o the amino acid neurotransmitters (glutamate and gamma-aminobutyric acid
[GABA])
o the neuropeptides (CRH and endorphins)
o acetylcholine
o Alterations in these areas appear to form the basis of psychiatric disease and are
the target for pharmacological treatment
Disturbances of Mental Function
Most occurrences are unknown
Known causes:
o drugs (e.g., lysergic acid diethylamide [LSD])
o long-term use of prednisone
o excess levels of hormones (e.g., thyroxine, cortisol)
o infection (e.g., encephalitis, acquired immunodeficiency syndrome [AIDS]), and
physical trauma
many ppl are predisposed
psychosocial stress
Physical disease
Thought that deficiency of norepinephrine or serotonin (or both) may serve as the
biological basis of depression
Changes in neurotransmitter release and receptor response can be both a cause and a
consequence of intracellular changes in the neurons involved
disorders such as schizophrenia are associated physiologically with excess transmission
of the neurotransmitter dopamine
neurotransmitter gamma-aminobutyric acid (GABA) seems to play a role in modulating
neuronal excitability and anxiety. Not surprisingly, many antianxiety (anxiolytic) drugs
act by increasing the effectiveness of this neurotransmitter, primarily by increasing
receptor responsiveness.
various areas of the brain are interconnected structurally and functionally by a vast
network of neurons
o particular neurotransmitter is often used by different neurons to carry out quite
different activities
MECHANISMS OF ACTION OF PSYCHOTROPIC DRUGS
Pharmacodynamics: concerned with the effects of drugs and the mechanism of their action
Pharmacokinetics:concerned with the movement of drugs within the body
absorption
distribution
metabolizing

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Pharmacogenetics is an approach to treatment that takes into consideration individual genetic
differences when determining which and how much medication to prescribe
Cause of mental or physical effects of the drugs taken many pts stop taking their
medications, or arent consistent w/ treatment --- barrier to successful treatment of mental
illness
Most psychotropic drugs act by either increasing or decreasing the activity of certain
neurotransmitterreceptor systems.
o Ex. Most drugs that were effective in reducing the delusions and hallucinations of
schizophrenia blocked the D2 dopamine receptors
concluded that delusions and hallucinations result from overactivity of
dopamine at these receptors.
Antianxiety & Hypnotic Drugs
Gamma-aminobutyric acid (GABA) is the major inhibitory (calming) NT in CNS
3 major receptors of GABA:
o GABAA
o GABAB,
o GABAC
The various subtypes of GABAA (1, 2, 3 )
Benzodiazepines
diazepam (Valium), clonazepam (Rivotril), and alprazolam (Xanax), bind to GABAA
receptors.
6 benzodiazapines used in Canada to treat insomnia
o lorazepam (Ativan), nitrazepam (Mogadon), oxazepam (Serax), temazepam
(Restoril), triazolam (Halcion), and flurazepam (Dalmane) - w/ hypnotic
(sleep-inducing) effects
o When combined with other CNS depressants, such as alcohol, opiates, or tricyclic
antidepressants (TCAs), the inhibi- tory actions of the benzodiazepines can lead to
life-threatening CNS depression.
o Ataxia is a common adverse effect secondary to the abundance of GABA
receptors in the cerebellum
o Possibility of dependence
Short-Acting Sedative-Hypnotic Sleep Drugs
Zopiclone (Imovane) newer class of hypnotic, termed a Z-drug,
o Unrelated to existing hypnotics; however it also promotes GABA and inhibits the
release of neurotransmitters.
o Onset of action is faster than most benzodiazepines
o Short half-life
o adverse effect unpleasant bitter taste upon awakening
o Should not be taken for more than 7 -10 consecutive days
o Prescription is required for use
Buspirone Hydrochloride (Bustab)

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 Used for short-term relief of excessive anxiety w/o having strong sedative-hyponotic
properties
Not a CNS depressant
No potential for dependence
Action not clearly understood seems to moderately enhance the effects of serotonin
An agonist ( blocks effect of the NT) & agonist
Adverse effects headache, dizziness, light-headedness, nausea, decreased
concentration, and insomnia
Treating Anxiety Disorder with Antidepressants
Selective serotonin reuptake inhibitors (SSRIs)
Increase both serotonin and norepinephrine,
Often used to treat:
o obsessive-compulsive disorder (OCD),
o social anxiety disorder (SAD)
o generalized anxiety disorder (GAD)
o panic disorder (PD)
o post-traumatic stress disorder (PTSD)
Venlafaxine hydrochloride (Effexor XR) is used to treat GAD, SAD, and PD.
Duloxetine hydrochloride (Cymbalta)-- major depressive disorder (MDD), for GAD, and
for neuropathic pain associated with peripheral neuropathy of diabetes, pain associated
with fibromyalgia, and chronic low back pain
Antidepressant Drugs
Evidence that seems to indicate that NT norepinephrine and serotonin play a major role in
regulating mood
3 hypotheses of antidepressants mechanism of action exist:
o The monoamine hypothesis of depression: suggests there is a deficiency in one or
more of the three neurotransmitters (serotonin, norepinephrine, or dopamine) The
theory is that increasing these neurotransmitters alleviates depression.
o The monoamine receptor hypothesis of depression: suggests that low levels of
neurotransmitters cause postsynaptic receptors to be up-regulated (increased in
sensitivity or number). Increasing of neurotransmitters by antidepressants results
in down-regulation (desensitization) of key neurotransmitter .Delayed length of
time for down-regulation may explain why it takes so long for antidepressants to
work, especially if they rapidly increase neurotransmitters.
o Antidepressant drugs increase production of neurotrophic factors with prolonged
use. These factors regulate the survival of neurons and enhance the sprouting of
axons to form new synaptic connections
Tricyclic Antidepressants (TCAs)
No longer considered first-line treatment for depression- hey have more adverse
effects, take longer to reach an optimal dose, and are far more lethal in overdose

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 Block the reuptake and destruction of serotonin and increase the synaptic level of this
neurotransmitter
Block reuptake of NE & SE
SSRIs
Fluoxetine hydrochloride (Prozac)
paroxetine hydrochloride (Paxil)
citalopram hydrobromide (Celexa),
escialopram oxalate (Cipralex),
fluvoxamine maleate (Luvox)
preferentially block the reuptake and destroy serotonin
Adverse effects: stimulation of diff serotonin receptors may inhibit the spinal reflexes of
orgasm, lead to apathy & low libido, & cause N&V
Serotonin-Norepinephrine Retake Inhibitors (SNRIs)
Increase SE & NE
Doses higher than 150mg/day can increase diastolic BP
Indicated for: acute & maintenance treatment of major depressive disorder, acute
treatment of generalized anxiety disorder, & managing neuropathic pain associated w/
diabetic peripheral neuropathy & for managing fibromyalgia
Serotonin & Norepinephrine Disinhibitors
Mirtazapine (Remeron)
o increases norepinephrine, dopamine, and serotonin (5-HT) transmission by
blocking central presynaptic 2 adrenergic inhibitory receptors.
o increased appetite resulting in weight gain being the most common adverse
effects. Patients may also experience orthostatic hypotension
Beginning of treatment with SSRIs, SNRIs, or SNDIsthere is a chance that the
medication may increase the risk of suicide or harm to others as a result of changing
serotonin levels in the brain
o Advantages: lower incidence of sexual dysfunction & antiemetic effects
patients should be weaned gradually over several weeks rather than abruptly due to the
risk of discontinuation symptoms. Ex. Dizziness, agitation
Monoamine Oxidase Inhibitors
Prevent destruction of monoamines by inhibiting the action of monoamine oxidase
Monoamines: organic compound and include the neurotransmitters norepinephrine, epinephrine,
dopamine, and serotonin etc
Monoamine oxidase (MAO) is an enzyme that destroys monoamines.
Monoamine oxidase inhibitors (MAOIs) inhibit the action of MAO and prevent the destruction
of monoamines

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Other Antidepressants

Mood Stabilizers
Lithium Carbonate
Ex. For ppl with bipolar disorder
It may be that an overexcitement of neurons in the brain underlies bipolar disorders and
that lithium carbonate interacts in some complex way with sodium and potassium at the
cell membrane to stabilize electrical activity
Adverse effect and toxicity result from its influence on electrical conductivity

Anticonvulsant Drugs
Valproate (Depakote, Depakene)
Show to be effective in the treatment of Bipolar disorders
Side effects: tremor, weight gain, and sedation
Base- line levels are measured for liver function indicators and complete blood count
(CBC) before an individual is started on this medication
Carbamazepine (Tegretol)
Useful in preventing mania & in tempering episodes of acute mania
Adverse effect: anticholinergic effects (e.g., dry mouth, constipation, urinary retention,
blurred vision), orthostatic hypotension, sedation, and ataxia
Lamotrigine (lamictal)
Effective drug for bipolar disorder
Good at treating depression of bipolar disorder
Other Anticonvulsants
Used as mood stabilizers

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 Gabapentin (Neurontin), topiramate (Topamax), and oxcarbazepine(trileptal)
Antipsychotic Drugs
Conventional Antipsychotics
1ST generation drugs- strong antagonists at D2 receptor
also receptors for Ach

Atypical Antipsychotics
produce fewer extrapyramidal effects
increases triglycerides
Clozapine
Risperidone
Quetiapine fumarate
Drug treatment for ADHD
methylphenidate hydrochloride
Drug treatment for Alzhemers Disease
anticholinesterase drugs

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