Drugs and Behaviour Midterm Flashcards
Psychopharmacology
Study of how drugs affect mood, perception, thinking, or behaviour.
Drug (Traditional)
Any substance that alters the body’s physiology
Drug (Contemporary)
Any substance that alters the body’s physiology but not food
Types of Drug Use
Instrumental: For a specific therapeutic purpose.
Recreational: Solely to experience effects.
Drug Naming Conventions
Generic
Trade
Chemical
Street
Generic Name
Non-proprietary name (e.g., Codeine)
Trade Name
Company-provided trademark name (e.g., Tylenol)
Chemical Name
Based on chemical structure (e.g., 3-Methoxymorphine)
Street Name
Slang given by users (e.g., Syrup)
Pharmacological Concepts
Dosage
Dose-Response Curve (DRC)
Potency
Effectiveness
Dosage
Reported in milligrams per body weight for comparison.
Dose-Response Curve
This is used to establish a true picture of physiological and behavioural effects if a drug
Important landmarks for dosing:
ED50: Median effective dose.
LD50: Median lethal dose.
Potency
Amount of drug required to produce an effect.
The lower the ED50 the higher the potency
Effectiveness
Ability of a drug to elicit a response, regardless of dose.
Types of Drug Effects
Objective Effects: Observable effects by others
Subjective Effects: Experienced effects, not observable
Pharmacokinetics
How drugs move and pass through the body
Absorption
Drug administration
Drug is absorbed into bloodstream
Refers to the passage of a drug from the site of administration to the bloodstream.
Distribution
Passage of drug from bloodstream into organs
Must penetrate membranes
Biotransformation
Drug broken down into metabolizes by enzymes
Phase 1 (water-soluble metabolites) and Phase 2 (conjugation).
Elimination
Drugs or metabolites or both are eliminated from body
Zero-order kinetics
Constant elimination rate.
First-order kinetics
Elimination dependent on drug concentration.
Pharmacodynamics
The physiological actions of drugs.
Therapeutic Index
Conveys the distance between toxic and therapeutic doses.
Therapeutic Window
Effective range for therapeutic drug effects.
Mechanism of Action (MoA)
How drugs influence neurotransmitter systems.
Ancient Origins of Neuropharmacology
Greek and Egyptian physicians explored drug effects.
Early 20th Century of Neuropharmacology
the development of chemical techniques allowed better drug study.
John B. Watson and Neuropharmacology
Focused on behaviours rather than subjective experiences, advancing research methods.
1950s Developments of Neuropharmacology
The success of antipsychotic medications (e.g., Chlorpromazine/Thorazine)
Peter Dews and Neuropharmacology
Demonstrated operant techniques (Skinner box) for studying drug effects.
Joseph Brady and Neuropharmacology
Linked behavioural and physiological effects of drugs, founding behavioural neuroscience.
Experimental Research
Establishes causal relationships using manipulated independent variables and measured dependent variables.
Controls in experimental research
Placebo groups and established drug groups.
Placebo Effect
The expectancy of receiving a drug can cause significant effects.
Non-Experimental Research
Correlational studies (e.g., smoking during pregnancy and infant mortality).
Cannot establish causation.
Measuring Drug Effects
in Animals
Conditioned Place Preference Tasks- Measure drug reward.
Self-Administration Task- Measure drug use tendency.
Measuring Drug Effects
in Human Behaviour
Subjective Effects: Self-reports of mood and feelings.
Motor Performance: Reaction time tasks.
Memory Tests: N-Back tasks for STM, recall tasks for LTM.
Drug Adaptation Mechanisms
Tolerance
Withdrawal
Dependence
Sensitization
Tolerance
Decreased drug effectiveness over time.
What are the different types of tolerance
Pharmacokinetic Tolerance
Pharmacodynamic Tolerance
Behavioural Tolerance
Behavioural Tolerance
Learned adaptation to drug effects.
Pharmacodynamic Tolerance
Receptor/circuit adaptation.
Pharmacokinetic Tolerance
Faster drug metabolism.
Withdrawal
Physical symptoms upon drug cessation.
Dependence
Necessity of drug use without implying addiction.
Sensitization
Increased behavioural effects following repeated drug administration.
Structural Imaging
MRI: High spatial resolution, but expensive.
Scanner uses a combination of strong magnetic fields and radio waves to produce detailed images of the inside of the body.
Functional Imaging
PET: Measures metabolic activity using radioactive tracers (poor temporal resolution).
fMRI: Measures the BOLD effect (oxygenated/deoxygenated blood ratio), offering better spatial and temporal resolution than PET.
Human brain
1.3 kg
Network of 100 billion Neurons with ~100 trillion synapses.
Central Nervous System
Brain (inside skull) and spinal cord (inside vertebral column).
Peripheral Nervous System
All nerves outside the CNS include 12 pairs of cranial and spinal nerves.
Bring information into the CNS and carry signals out of the CNS
Divided into 2 subdivisions:
Somatic nervous system
Autonomic nervous system
Nerve vs. Tract
Nerves are bundles of axons outside the CNS; tracts are bundles of axons within the CNS.
Afferent Nerves vs. Efferent Nerves
Afferent nerves carry signals toward a region; efferent nerves carry signals away.
Ganglion vs. Nucleus
Ganglia are clusters of neuron cell bodies outisde the CNS
Nuclei are clusters of neuron cell bodies inside the CNS
Somatic Nervous System
Function: Interacts with the external environment.
Sensory: Receives information from skin, eyes, ears, etc.
Motor: Controls skeletal muscles.
Autonomic Nervous System
Function: Regulates internal organ function.
Sensory & Motor: Uses two-neuron pathways.
Autonomic Nervous System Subdivisions
Sympathetic: fight or flight
Parasympathetic: promotes relaxation
Sympathetic
Originates in thoracic and lumbar regions.
“Fight or flight” responses increase heart rate and breathing, dilate pupils, and inhibit digestion.
Parasympathetic
Originates in cranial and sacral regions.
“Rest and restore” responses: decreases heart rate and breathing, constricts pupils, stimulates digestion.
Physical Protection of the CNS
Bones
Meninges
Cerebrospinal Fluid
Bones
Skull protects the brain; vertebrae protect the spinal cord.
Meninges
Three layers encasing the CNS:
Dura mater: Tough, outer membrane.
Arachnoid membrane: Web-like middle layer.
Pia mater: Thin, adheres to CNS surface.
Cerebrospinal Fluid
Fills the subarachnoid space and ventricular system.
Functions as a shock absorber and nutrient exchange medium.
Structure of a Neuron
Soma (Cell Body): Contains the nucleus and organelles.
Dendrites: Receive signals from other neurons.
Axon: Transmits electrical signals (action potentials).
Axon Terminals: Release neurotransmitters at synapses.
Synapse: Junction where communication between neurons occurs.
Glial Cells
Serve to support the functions of neurons (i.e., supporting cells)
Have many functions in the nervous system
e. g., structural support, insulation, nourishment
Glial Cell Type
Oligodendrocytes: Myelinate CNS axons.
Schwann cells: Myelinate PNS axons.
Astrocytes: Support, repair, and help form the BBB.
Microglia: Act as immune cells in the CNS.
Spinal Cord Structure
Gray Matter: Central region containing neuron cell bodies (dorsal horns for sensory; ventral horns for motor).
White Matter: Surrounding area of myelinated axons.
Spinal Nerves: 31 pairs (Cervical: 8, Thoracic: 12, Lumbar: 5, Sacral: 5, Coccygeal: 1).
Brain Regions
Hindbrain
Midbrain
Forebrain
Telencephalon
Hindbrain Components
Medulla (Myelencephalon): Contains reticular formation; regulates vital functions (breathing, heart rate).
Pons (Metencephalon): Involved in sleep, arousal, and motor control.
Cerebellum: Coordinates motor control and balance.
Midbrain Components
Tectum: where visual and inferior auditory are processed .
Tegmentum: Contains structures like the periaqueductal gray (pain modulation), substantia nigra, and red nucleus (motor control).
Forebrain Components
Diencephalon:
Thalamus: Sensory relay station.
Hypothalamus: Regulates homeostasis and autonomic functions.
Telencephalon:
Cerebral Cortex: Outer layer; involved in higher cognition, sensory processing, motor function.
Subcortical Structures:
Basal Ganglia: (Amygdala, caudate nucleus, putamen, globus pallidus) - Involved in voluntary movement.
Limbic System:
(Hippocampus, amygdala, fornix, cingulate cortex, septum, mammillary bodies) - Involved in emotion, memory, and motivation.
Neurotransmission & Neurotransmitters General Process
Synthesis: Neurotransmitters are produced in the neuron.
Release: Stored in vesicles and released in response to an action potential.
Receptor Binding: Bind to receptors on the postsynaptic cell.
Termination: Removed or deactivated to end the signal.
Drug Actions on Neurotransmission
Agonists: Bind to receptors and mimic the neurotransmitter’s effects.
Antagonists: Bind to receptors and block the neurotransmitter’s effects.
What Are Drugs of Abuse
Although drugs of abuse have diverse mechanisms of action, they all converge on the brain’s reward pathways.
Outcome:
Result in compulsive use despite adverse consequences.
Addiction
The compulsive use of a substance despite significant negative consequences.
Addiction and the Impact on the Brain
Disrupts regions responsible for reward, motivation, learning, judgment, and memory.
DSM Criteria (Substance Use Disorder - SUD)
Impaired Control: Using more than intended; inability to cut down.
Social Problems: Neglecting responsibilities and relationships.
Risky Use: Use in dangerous situations despite known risks.
Physical Dependence: Tolerance (needing more for the same effect) and withdrawal symptoms.
Contributing Factors to Addiction
Genetic/Epigenetic Factors
Brain Function
Psychological Factors
Social & Sociocultural Factors
Genetic/Epigenetic Factors related to Addiction
Genetic predispositions (e.g., variations in dopamine receptor genes).
Epigenetic modifications (e.g., histone variant changes affecting withdrawal).
Brain Function related to Addiction
Potentiation of the reward circuit, particularly in the mesolimbic dopaminergic system.
Psychological Factors related to Addiction
Positive and negative reinforcement.
Expectancy effects.
Coping with stress, trauma, or major life transitions.
Social & Sociocultural Factors related to Addiction
Childhood maltreatment, victimization.
Permissive attitudes among family/peers.
Influences during adolescence and through advertising.
Historical Perspectives on Addiction
Initially seen as a moral failing.
Shifted focus from purely physical dependence (withdrawal symptoms) to a broader understanding involving psychological and neurobiological factors.
Modern Views on Addiction
Considered a disorder or disease influenced by both biological and environmental factors.
Research using animal models helped validate self-administration and the reinforcing properties of drugs.
Mechanisms of Motivation & Reinforcement
Doapmine release
Liking vs. Wanting (Berridge Model): enjoyment and than wanting is craving, related to dopamine
Ex: cocaine users may not want the drug but they need it cuse they dont want to go through withdrawl.
Reward Circuitry
Key Structures: Ventral tegmental area (VTA) and nucleus accumbens.
Dopamine’s Role: Central in signaling and reinforcing rewarding stimuli.
Activation & Guidance
Activation: Imbalances in the system trigger dopamine release.
Guidance: Sensory inputs and learned experiences shape goal-directed behaviors.
Liking vs. Wanting (Berridge Model)
Liking: The pleasure/hedonic aspect (linked to endogenous opioids).
Wanting: The incentive or motivational drive (linked to dopamine).
In addiction, “wanting” may persist even when “liking” (actual enjoyment) diminishes.
Disease Model
Views addiction as a brain disorder resulting from genetic and environmental factors that alter brain function.
Drive Theory
Proposes that repeated drug use builds a motivational drive to seek the positive reinforcing effects.
Opponent Process Theory
Acute drug use produces a euphoric (Process A) effect that is counteracted by a delayed dysphoric (Process B) response. Over time, the opposing process may intensify, contributing to addiction.
Incentive-Salience Model
Addiction develops when an individual shifts from “liking” the drug effects to “wanting” them, even if the pleasurable impact decreases.
Triggers for Drug Use
Environmental Triggers:
Specific locations, social settings, peer pressure, traumatic events, and even the presence of drug paraphernalia.
Physiological Triggers:
Cravings due to neurotransmitter downregulation or pain management issues.
Psychological Triggers:
Mood disorders such as depression, anxiety, paranoia, and hallucinations.
Consequences of Addiction
Physical:
Withdrawal symptoms, kidney or heart failure, tissue decay.
Psychological:
Mood disorders, paranoia, and other mental health issues.
Social:
Financial, interpersonal, and broader community impacts.
Treatment Options Step 1
Step 1: Medical/Pharmacological Interventions
Detoxification: Medically managed withdrawal.
Medication Approaches:
Agonist Substitution: Use a safer substitute (e.g., methadone).
Antagonist Treatment: Block the drug’s effects (e.g., naltrexone).
Aversive Treatment: Induce unpleasant effects when the drug is used (e.g., disulfiram/Antabuse).
Treatment Options Step 2
Step 2: Behavioral and Psychosocial Interventions
12-Step Programs: Such as Alcoholics Anonymous (AA) and Narcotics Anonymous (NA), focus on acceptance, surrender, and active involvement.
Personalized Treatment Programs: Tailored to individual needs, combining medications with psychological therapies.
Relapse Prevention & Harm Reduction: Continuous reassessment and support to minimize relapse risk.
Psychostimulants
Psychostimulants are common drugs of abuse, but many psychostimulant drugs have legitimate therapeutic purposes.
The drugs have different mechanisms but have an effect on different receptors in the brain.
While positive effects like alertness and sexual ability have been reported, the detrimental side effects include cardiac illness and even psychosis.
Administration Routes
Rapid absorption methods are preferred (intravenous injection, snorting/insufflation, inhalation).
Distribution
Psychostimulants cross both the blood–brain and placental barriers.
Cocaine tends to concentrate in the brain; methamphetamines also reach high levels in the kidneys and lungs.
Neurotransmission Basics
Monoamines—dopamine, norepinephrine, and serotonin—are chemical messengers in the brain. When a neuron sends a signal, these chemicals are released into a tiny gap between neurons called the synaptic cleft. They bind to receptors on the next neuron to pass along the signal.
Termination of action occurs via enzymes (MAO, COMT) and reuptake transporters (DAT, NET, SERT).
Self-Administration & Discriminative Stimulus in Animals
Animals (rats, pigeons, primates) will self-administer psychostimulants.
Drugs like amphetamine and cocaine produce recognizable discriminative cues.
Behavioural Changes:
Unconditioned Responses: Increased locomotion, exploration; at high doses, signs like auto-mutilation in primates.
Conditioned Responses: Rate dependency effects (e.g., learned behaviours affected by drug state).
Effects on Behavior in Humans
Physiological Effects:
Increased heart rate, blood pressure, and body temperature.
Pupil dilation, vasodilation, and bronchodilation.
Decreased appetite.
Behavioural Effects:
Enhanced purposeful (goal-directed) and purposeless behaviours.
Stereotyped or repetitive behaviors.
Subjective Effects:
Euphoria, increased energy, alertness, and sense of well-being.
Heightened sexual desire; some users experience anxiety.
Insomnia and altered sensory perceptions (e.g., tunnel vision, time distortion).
Impaired driving ability and increased risk of accidents.
Patterns of Use for Cocaine and Amphetamines
Cocaine: Long history of self-administration; often used with other substances.
Amphetamines: Generally sporadic use, often associated with recreational “speed” culture.
Harmful & Toxic Effects of Drug Use
General Toxicity: Liver damage, mucosal injuries (from cocaine), blurred vision, weight loss, and attention deficits.
Neurotoxicity: Long-term damage to dopamine and serotonin neurons, affecting brain regions such as the hippocampus and prefrontal cortex.
Specific Issues:
Methamphetamine is linked to cardiac issues, skeletal muscle deterioration, skin-picking behaviours, dental problems, and psychosis.
High doses/extended use can lead to “monoamine psychosis,” resembling schizophrenia.
Tolerance
Acute tolerance develops to positive subjective effects.
Appetite suppression may dissipate after approximately 2 weeks.
Increased dosage required for the same effect; risk of more severe toxic effects.
Dependence & Withdrawal
Dependence can manifest in various forms.
Withdrawal from cocaine is rapid but not usually medically severe, whereas amphetamine withdrawal can be challenging and may involve suicidal ideation in heavy users.
Detoxification
Removal of the drug from the body; relapse is common due to the reinforcing nature of even a single dose.
Behavioral Therapies
Cognitive-behavioral therapy, contingency management, and community reinforcement strategies.
Pharmacotherapy
Modafinil: Stimulates dopamine, norepinephrine, and glutamate systems.
Methylphenidate: Sometimes used as a replacement therapy for amphetamines.
Pharmacogenetics
This is how genetic differences influence a drugs pharmacokinetic and pharmacodynamic effects/properties.
What are the stages of pharmacokinetics
Absorption
Distribution
Biotransformation
Elimination
pKa
Its a fancy way to measure how well a drug is absorbes
Measures how acidic a drug is
Lower pKa indicates higher acid
What role does pKa play in absorption
The pKa affects how well drugs are absorbed in the body.
If a drug’s pKa is close to the local pH where it is administered, the drug is generally absorbed more easily
Blood brain barrier
Tight junctions prevent pathogens, hormones, and other substances from entering the brain.
Nutrients and other important molecules pass through this barrier through eitherpassive diffusionoractive transport.
Passive Diffusion
Drug should be lipid (or fat) soluble
Drug should be uncharged
Drug should be relatively small
Active transport
Larger and/or polar/charged molecules
Biotransformation Phase 1
First biotransformation phase for a drug that normally involves P450 enzymes and produces a water-soluble metabolite
Biotransformation Phase 2
Second biotransformation phase occurring through conjugation of a drug’s metabolites, making them resistant to passive diffusion
Active Metabolites
Some metabolites of drugs offer physiological effects of their own.
Prodrugs
Inactive forms of drugs that turn into activated drugs in the body
Half life
The time it takes for the body to eliminate half of a given blood level of a drug.
Somatic Nervous System
Interacts with the body’s external environment (body surface and muscles)
Receives sensory information from sensory organs (e.g., skin, eyes, ear, etc) and controls movements of skeletal muscles
Autonomic Nervous System
Interacts with the body’s internal environment (internal organs)
The ventricular system
Series of chambers filled with CSF.
Four ventricles in the brain. two lateral, one third, one fourth ventricle.
CSF Functions
Acts as a shock absorber (mechanical cushion that ‘reduces’ the weight of the brain)
Provides an exchange medium between blood and brain (nutritional support)
Cells of the nervous system
Neurons and Glia
Neurons
Specialized cells for the reception, conduction, and transmission of electrochemical signals
Many sizes and shapes
Action Potential
The neuron is normally at rest with a negative charge inside compared to the outside
Triggering the Action Potential:
A stimulus causes the neuron’s membrane potential to become less negative.
When the potential reaches a specific threshold, it triggers the action potential
Depolarization
Voltage-gated sodium (Na⁺) channels open.
Sodium ions rush into the neuron, making the inside more positive
Repolarization:
After the peak, voltage-gated potassium (K⁺) channels open.
Potassium ions exit the neuron, which helps to bring the membrane potential back to a negative value.
Resetting the Neuron:
The sodium-potassium pump restores the original ion balance, returning the neuron to its resting state
Neurotransmitters
These are mostly small molecules that are stored in vesicles and are released following an action potential.
Neuropeptides
Generally large signalling molecules.
Chains of amino acids that are often co-released in specific neuronal subtypes.
Neurohormones
Transmitter substances that have hormonal effects
Glutamate
This is the major excitatory neurotransmitter in the CNS.
Mediates 70% of signalling in CNS.
Acts on kinate, AMPA and NMDA receptors.
Gaba
This is the major inhibitory transmitter in the brain
Bind to two types of receptors to cause inhibitory signal.
GABA A receptors:
Ionotropic receptors that allow influx of Cl-
GABA B receptors
Metabotropic receptors
Glycine
Also, an inhibitory neurotransmitter
Exists predominantly in lower brain stem and spinal cord.
Acetylcholine
This transmitter plays an important role in:
Cortical activation
Learning and memory
Indirectly in reward and sleep
Serotonin
This transmitter plays an important role in:
Mood
Aggression
Sleep-wake cycles
Dreaming
Appetite
