BIOLOGICAL PSYCHOLOGY

Second Term (Midterm Exam)

PSYCHOPHARMACOLOGY: CHAPTER 3
Psychopharmacology – the study of the use of
medications in treating mental disorders
Neurotransmitters – act on neurons in their own
immediate vicinity, generally at a synapse; the
chemical messengers that travel from one brain cell
to another and are synthesized by enzymes from
certain dietary amino acids or precursors;
substances released by one cell at a synapse that
produce a reaction in a target cell
Synaptic Transmission
Transmitter substances are:
Scientists gave identified more that 60 distinct types
 Synthesized, stored, released, bound and of neurotransmitters in the human brain
terminated
 Susceptible to drug manipulation Most common neurotransmitters are:

Receptors – molecules situated on the cell 1. Acetylcholine (ACH)

membrane that are binding sites for 2. Dopamine
neurotransmitters 3. Glutamate
4. Serotonin
Agonist – a drug that binds to and activates a 5. Norepinephrine
receptor 6. Gamma-Aminobutyric Acid (GABA)
Antagonist – a drug that binds to but does not Acetylcholine (ACH)
activate (block) a receptor
Acetylcholine – learning neurotransmitter; ester of
3 Rules of Neurotransmission choline and acetic acid; the first neurotransmitter
1. What goes up, must come down (intoxication- discovered; can be found in all motor neurons
withdrawal) (efferent neurons), which stimulate muscles to
2. Neurotransmitters are not easily fooled (Up- contract; the chief neurotransmitter in the
regulation-Down-regulation) (Drug tolerance and parasympathetic nervous system (rest and digest);
withdrawal) commonly associated with memory, cognition,
3. With great power comes great responsibility attention, and sleep/wake
(more efficacy-more severe side effects) Cholinergic Neurons – neurons that use
Types of Neurotransmitters acetylcholine as their major neurotransmitter

1. Small-Molecule Transmitters – one of a group Cholinergic Receptors: nicotinic receptors and

of chemical messengers that includes amino muscarinic receptors
acids and amines Locations: (1) neuromuscular junction, (2)
2. Neuropeptides – a peptide that acts as a preganglionic autonomic synapses, (3)
neurotransmitter, a neuromodulator, or postganglionic parasympathetic synapses, (4) basal
neurohormone forebrain projections to hippocampus and amygdala,
3. Gaseous Neurotransmitters (5) the septum, and (6) the brainstem

 ↓ Heart rate

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BIOLOGICAL PSYCHOLOGY
Second Term (Midterm Exam)

 ↑ Secretions (sweat, saliva) Parkinson’s disease, addiction, schizophrenia, and

 ↑ Memory other neuropsychiatric disorders
 ↑ Muscle contractions
Increased Dopamine Levels:
Drugs that increase or mimic: (1) Nicotine, (2)
 Positive Effects: enhance mood, motivation,
Muscarine, and (3) Alzheimer’s drugs
and focus; it's associated with feelings of
Drugs that decrease or block: (1) Botox, and (2) pleasure and reward, which can reinforce certain
Anticholinergics behaviors
 Negative Effects: schizophrenia, which can
Increased Acetylcholine Levels: cause hallucinations, delusions, and disordered
 Muscular Effects: High levels of acetylcholine thinking. It may also contribute to impulsivity and
can lead to excessive stimulation of muscles, addiction behaviors; Movement Disorders-
potentially causing spasms or tremors. involuntary movements, like tardive dyskinesia
 Parasympathetic Overdrive: An increase can Decreased Dopamine Levels:
overstimulate the parasympathetic nervous
system, potentially causing bradycardia (slow  Parkinson's Disease: characterized by
heart rate), salivation, lacrimation (tear tremors, stiffness, and difficulty with balance and
production), urination, digestion issues, and coordination. This is due to the loss of dopamine-
miosis (constricted pupils). producing neurons in a part of the brain called
 Cognitive and Mood Effects: While the substantia nigra.
acetylcholine is crucial for learning and memory,  Depression: including lack of motivation,
an excess might be associated with anxiety and fatigue, and feelings of hopelessness.
other mental health issues  Cognitive Effects: difficulties with
concentration, memory, and problem-solving
Decreased Acetylcholine Levels: skills.
 Myasthenia Gravis: This autoimmune disease Locations: Dopaminergic neurons in the midbrain
is characterized by the destruction of project to the: (1) Substantia nigra and basal ganglia,
acetylcholine receptors, leading to muscle (2) Ventral tegmentum projections to hippocampus,
weakness and fatigue. amygdala, and nucleus accumbens, and (3) Ventral
 Alzheimer’s Disease: A notable decrease in tegmentum projections to frontal lobe of the cortex
acetylcholine has been observed in patients with
Alzheimer’s, leading to cognitive decline,  ↑ Alertness
memory loss, and difficulties with learning.  ↑ Happiness
 Parasympathetic System Effects: Reduced  ↓ Hunger
acetylcholine can impair parasympathetic
Drugs that increase or mimic: (1) cocaine, and (2)
nervous system functions, potentially leading to
Parkinson’s drugs
issues like constipation, difficulties with bladder
control, and dry mouth and eyes Drugs that decrease or block: antipsychotics
Dopamine Glutamate (Glu)
Dopamine – pleasure chemical; chemical released Glutamate – Memory; most excitatory
in the brain that makes you feel good; released when neurotransmitter in the cortex; most abundant free
mammals receive a reward in response to their amino acid in the brain and is at the crossroad
behavior; involved with motivation, decision-making, between multiple metabolic pathways; too much =
movement, reward processing, attention, working excitotoxicity (death of neurons) and Parkinson’s
memory, and learning; plays an important role in

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BIOLOGICAL PSYCHOLOGY
Second Term (Midterm Exam)

disease, Alzheimer’s disease, and Huntington’s Serotonin - Calming Chemical; best known for its
disease; important to learning and memory mood modulating effects; lack = depression and
related neuropsychiatric disorders; helping to
Locations:
manage appetite, sleep, memory, and, most
 Glutamate is recycled and made by glial cells in recently, decision-making behaviors
your brain Increased Serotonin Levels:
 Widely distributed in the central nervous system
 help form memories, occurs in glutamatergic  Positive Effects: At optimal levels, increased
neurons in the hippocampus and cortex. serotonin is associated with improved mood,
 Among the 20 basic amino acids that are used to feelings of happiness, and increased overall
build other proteins sense of well-being.
 Serotonin Syndrome: However, excessively
Drugs that increase or mimic: (1) D-cycloserine, high levels of serotonin can lead to a potentially
and (2) domoic acid (shellfish) life-threatening condition known as serotonin
Drugs that decrease or block: (1) Namenda (for syndrome. Symptoms include high body
Alzheimer’s), and (2) dextromethorphan temperature, agitation, increased reflexes,
(Robitussin) tremor, sweating, dilated pupils, and diarrhea. It's
often caused by drug interactions or overdose of
Increased Glutamate Levels: serotonin-increasing medications.
 Other Effects: High levels might also lead to
 Excitotoxicity: High levels of glutamate can
anxiety, restlessness, and gastrointestinal
overstimulate neurons, potentially leading to
issues.
neuronal damage or death. This phenomenon,
known as excitotoxicity, is implicated in various Decreased Serotonin Levels:
neurodegenerative diseases, including
Alzheimer's, multiple sclerosis, and Parkinson's  Depression and Mood Disorders: Low levels
disease. of serotonin are commonly associated with
 Seizures: Excessive glutamate activity can depression, mood swings, and other mood
contribute to the development of seizures. disorders. Serotonin's role in mood regulation is
 Psychiatric Disorders: Some studies suggest a key reason why many antidepressants focus
that elevated glutamate levels may be on increasing serotonin levels.
associated with certain psychiatric disorders,  Sleep Problems: Serotonin is a precursor to
such as anxiety or depression. melatonin, the hormone that regulates sleep-
wake cycles. Therefore, low serotonin can
Decreased Glutamate Levels: disrupt sleep patterns.
 Appetite and Digestion Issues: Given
 Cognitive Impairment: Reduced glutamate
serotonin's role in regulating appetite and
levels can lead to cognitive difficulties, affecting
digestion, reduced levels can lead to changes in
learning and memory processes.
eating habits and gastrointestinal problems.
 Psychiatric Effects: Lower levels of glutamate
 Cognitive Impairments: Insufficient serotonin
have been linked to conditions like schizophrenia
can affect memory and cognitive function.
and depression.
 Neurological Disorders: Some research Drugs - an “exogenous” chemical that significantly
suggests that diminished glutamate activity may alters the function of certain bodily cells when taken
play a role in neurodegenerative diseases like in relatively low doses (chemical is not required for
Parkinson's disease. normal cellular functioning); can exert antagonistic
effects by interfering with the synthesis pathways of
Serotonin (5-HT)

Reviewer Prepared by: Loraine Mae D. Quinto (PSY 233)

BIOLOGICAL PSYCHOLOGY
Second Term (Midterm Exam)

neurotransmitters; medication to treat a disease; a 9. Intracerebroventricular – directly into the

chemical that is likely to be abused cerebrospinal fluid in cerebral ventricles
Neurotransmitter Production Drug Effectiveness

 Manipulating the synthesis of a neurotransmitter 1. Dose-response (DR) curve – depicts the

will affect the amount available for release. relation between drug dose and magnitude of
 The simplest way to boost the rate of drug effect
neurotransmitter synthesis is to provide larger 2. Efficacy – refers to the maximal therapeutic that
quantities of the basic building blocks, or a drug can achieve
precursors, for the neurotransmitter 3. Potency – describes the amount of the drug
needed to achieve the maximum effect
Neurotransmitter Storage 4. Half-life – the time taken for half of the drug to
 Certain drugs have an antagonistic effect by be removed from the blood stream
interfering with the storage of neurotransmitters Tolerance and Withdrawal
in vesicles within the neuron.
 E.g., Reserpine – treats blood pressure but  Repeated drug administration results in
often produces depression because it interfered diminished drug effect (or requires increased
with the uptake of monoamine serotonin dosage to maintain constant effect
 Withdrawal effects are often the opposite of the
Pharmacokinetics – the study of drug absorption, drug effect and often accompanies tolerance
distribution within body, and drug elimination  Tolerance can reflect decreased drug-receptor
 Drug molecules interact with target sites to affect binding or reduced postsynaptic action of the
the nervous system drug
 The drug must be absorbed into the bloodstream Placebo Effect – refers to the phenomenon where
and then carried to the target site(s) individuals experience a perceived improvement in
 Absorption depends on the route of their condition or symptoms after receiving a
administration treatment that has no therapeutic effect; this
 Drug distribution depends on how soluble the improvement is not attributed to the active
drug molecule is in fat (to pass through ingredients of the treatment but rather to the
membranes) and on the extent to which the drug individual’s belief in the effectiveness of the
binds to blood proteins (albumin) intervention
 Drug elimination is accomplished by excretion
into urine and/or by inactivation by enzymes in The Hazards of Drugs
the liver Addiction – the compulsive need to use the drug
Basic Principles of Drug Effects repeatedly

Administration of Drugs  Causes – the ability of a drug to stimulate our

natural neural systems of reward, which we
1. Intravenous (IV) – into a vein (rapid absorption) experience as feelings of pleasure
2. Intraperitoneal (IP) – into the gut (used in lab  Nucleus Accumbens – a dopaminergic
animals) and chemotherapy structure believed to participate in reward and
3. Subcutaneous (SC) – under the skin addiction
4. Intramuscular (IM) – into a muscle  Treatment – medications, vaccination, therapy
5. Topical – absorbed through the skin
6. Oral – via the mouth Psychoactive drugs are usually administered to
7. Inhalation – inhalation of the drug into the lungs obtain a particular psychological effect. By definition,
8. Intracerebral – into part of brain these drugs circumvent the protective systems of the

Reviewer Prepared by: Loraine Mae D. Quinto (PSY 233)

BIOLOGICAL PSYCHOLOGY
Second Term (Midterm Exam)

blood–brain barrier to gain access to the central  Higher doses produce symptoms that are
nervous system. similar to schizophrenia (hallucinations,
particularly in the form of tactile sensations
Effects & Types of Medications used for Various
such as feeling bugs on the skin)
Mental Disorders
Cocaine:
1. Stimulants – class of drugs that increase activity
in the brain and central nervous system, leading  Cocaine is a powerful, addictive dopamine
to increased alertness, attention, and energy; agonist derived from the leaves of the coca
they are commonly used to treat Attention Deficit plant of South America.
Hyperactivity Disorder (ADHD) and sometimes  Cocaine acts as a dopamine reuptake
narcolepsy inhibitor
Caffeine:  Behavioral effects: euphoria; excitement
Amphetamine:
 A stimulant drug found in coffee, tea, cola,
and chocolate  Amphetamine is a highly addictive drug that
 Antagonist for adenosine (relaxes and acts as a potent dopamine agonist.
dilates blood vessels)  Behavioral effects: alertness; appetite
 Increases blood pressure and heart rate, suppression; “rush
arousal, reduces headache, improves  Amphetamine has a dual action at synapses
concentration, and wards off sleepiness that use dopamine and norepinephrine
 Withdrawal symptoms- fatigue, headache,  Methamphetamine – a variation of
cardiac arrhythmias amphetamine that is cheaply produced and
 Pregnant and nursing women (crosses to widely abused in the United States.
placenta easily)
 Correlated with lower rates of Parkinson's Ecstasy (MDMA):
disease  A close relative of amphetamine that
Nicotine: produces its behavioral effects by stimulating
the release of serotonin
 smoking or chewing tobacco  acts as both a stimulant and psychedelic
 increases heart rate and blood pressure,  alters mood and produces an energizing
promotes the release of adrenaline into the effect, as well as distortions in time and
circulation, reduces fatigue, alertness, perception and enhanced enjoyment from
muscular relaxation and heightens cognitive tactile experiences.
performance  Withdrawal symptoms – fatigue, loss of
 agonist at the nicotinic cholinergic receptor appetite, depressed feelings, trouble
 stimulates dopaminergic neurons in the concentrating
nucleus accumbens (source of the addictive
properties of nicotine) 2. Antidepressants – Depression affects various
 withdrawal symptoms – inability to systems of the body and brain, and its response
concentrate and restlessness to antidepressants is debated; Antidepressants
typically take at least four weeks to show effects
Cocaine and Amphetamine: like improved appetite, motivation, and energy;
Some antidepressants may promote brain nerve
 These drugs are among the most addictive
cell growth, enhancing cognitive and behavioral
drugs known.
adaptability.
 Lower doses produce alertness, elevated
mood, confidence, and a sense of well-being.

Reviewer Prepared by: Loraine Mae D. Quinto (PSY 233)

BIOLOGICAL PSYCHOLOGY
Second Term (Midterm Exam)

Selective Serotonin Reuptake Inhibitors  Inhibit monoamine oxidase, an enzyme that

(SSRIs): breaks down serotonin, norepinephrine, and
dopamine.
 Increase levels of serotonin in the brain by
 Examples: Phenelzine (Nardil),
blocking its reabsorption (reuptake) into
tranylcypromine (Parnate).
neurons.
 Uses: Typically used as a last resort due to
 Examples: Fluoxetine (Prozac), sertraline
dietary restrictions and side effects.
(Zoloft), citalopram (Celexa), escitalopram
 Side Effects: Hypertensive crisis with
(Lexapro).
certain foods, weight gain, insomnia,
 Uses: First-line treatment for depression,
dizziness.
anxiety disorders, PTSD, OCD.
 Side Effects: Nausea, insomnia, sexual Example: tranylcypromine (Parnate),
dysfunction, weight gain, dry mouth. phenelzine (Nardil)
Example: fluoxetine (Prozac), sertraline (Zoloft), Atypical Antidepressants:
citalopram (Celexa)
 Differ from other classes, work in various
Serotonin and Norepinephrine Reuptake ways on neurotransmitters.
Inhibitors (SNRIs):  Examples: Bupropion (Wellbutrin),
mirtazapine (Remeron), trazodone.
 Mechanism: Similar to SSRIs but also affect
 Uses: Depression, sometimes used to help
norepinephrine.
with smoking cessation (bupropion) or
 Examples: Venlafaxine (Effexor XR),
insomnia (trazodone, mirtazapine).
duloxetine (Cymbalta), desvenlafaxine
 Side Effects: Varies; bupropion is less likely
(Pristiq).
to cause sexual dysfunction but can increase
 Uses: Depression, anxiety, chronic pain
seizure risk.
disorders.
 Side Effects: Similar to SSRIs, plus Example: bupropion (Wellbutrin), mirtazapine
increased blood pressure. (Remeron)
Example: enlafaxine (Effexor), duloxetine 3. Anxiolytics – Anxiety is a prevalent psychiatric
(Cymbalta) condition, treated with drugs known as
"anxiolytics."; These drugs primarily work by
Tricyclic Antidepressants (TCAs):
affecting the neurotransmitter gamma-
 Block the reabsorption of serotonin and aminobutyric acid (GABA); Anxiolytics vary in
norepinephrine. Older class of how quickly they alleviate symptoms and the
antidepressants. duration of their effects
 Examples: Amitriptyline, nortriptyline Benzodiazepines:
(Pamelor), imipramine (Tofranil).
 Uses: Depression, sometimes used for  Enhance the effect of the neurotransmitter
chronic pain. gamma-aminobutyric acid (GABA), leading
 Side Effects: More severe than to sedation, muscle relaxation, and reduced
SSRIs/SNRIs, including dry mouth, blurred anxiety.
vision, constipation, urinary retention,  Examples: diazepam (Valium), lorazepam
cardiac toxicity. (Ativan), alprazolam (Xanax). Used for short-
term relief of severe anxiety.
Example: amitriptyline, nortriptyline (Pamelor)  Usage: Effective for short-term relief of
Monoamine Oxidase Inhibitors (MAOIs): severe anxiety and panic attacks. Often used
on an as-needed basis.

Reviewer Prepared by: Loraine Mae D. Quinto (PSY 233)

BIOLOGICAL PSYCHOLOGY
Second Term (Midterm Exam)

 Side Effects: Sedation, dizziness,

weakness, unsteadiness. Risk of
dependence and withdrawal symptoms with
long-term use.
Selective Serotonin Reuptake Inhibitors:

 Primarily used as antidepressants, they also

increase serotonin levels in the brain and can
help reduce anxiety.
 Examples: Escitalopram (Lexapro),
sertraline (Zoloft), fluoxetine (Prozac).
 Usage: First-line treatment for chronic
anxiety disorders due to a more favorable
side effect profile.
 Side Effects: Nausea, sexual dysfunction,
headache, insomnia, nervousness.
Serotonin-Norepinephrine Reuptake
Inhibitors (SNRIs):

 Increase both serotonin and norepinephrine

levels.
 Examples: Venlafaxine (Effexor), duloxetine
(Cymbalta).
 Usage: Used for generalized anxiety
disorder and other anxiety disorders.
 Side Effects: Similar to SSRIs, plus possible
increased blood pressure.
4. Moon Stabilizers – used to treat mood disorders
characterized by intense and sustained mood
shifts; balance mood swings and maintain a
more stable emotional state; manage both manic
and depressive episodes; Lithium is one of the
most well-known and traditionally used mood
stabilizers; anticonvulsants such as valproate
(Depakote), lamotrigine (Lamictal), and
carbamazepine (Tegretol).
Side Effects: (1) increase weight gain, (2)
drowsiness, (3) tremors, (4) gastrointestinal
issues, and (5) – kidneys and thyroid
Adjunctive Therapy: (1) psychotherapy, (2)
lifestyle changes, and (3) antidepressants or
antipsychotics

Reviewer Prepared by: Loraine Mae D. Quinto (PSY 233)