Chapter 3 — The Bases Of Human Behaviour

Fig 1 — Educational Diagram: Introduction: The bases of human behaviour

What it means
The phrase "bases of human behaviour" refers to the multiple factors and systems that produce, shape and influence how people think, feel and act. These bases are interrelated and include biological, psychological and socio‑cultural influences. Modern psychology uses an interactionist view: behaviour is the product of the person (biology, cognition, emotions) and the environment (social, cultural, situational).

Major bases

1. Biological bases
Genetics, brain structures, neural circuits, neurotransmitters and hormones form the biological substrate of behaviour. Genes provide a range of potential, the nervous system implements processing, and endocrine signals modulate arousal, mood and stress responses. Example mechanisms: prefrontal cortex and decision‑making, amygdala and fear processing, dopamine and reward‑seeking.

2. Psychological (cognitive & emotional) bases
Cognitive processes (attention, memory, perception, reasoning) and emotions shape how stimuli are interpreted and which responses are chosen. Learning (classical/operant conditioning, observational learning) changes behaviour through experience. Motivation (biological drives, goals, incentives) directs behaviour over time.

3. Social and cultural bases
Family, peers, social norms, cultural values and institutions influence behaviour patterns, beliefs and expectations. Social learning and socialization teach appropriate responses; cultural scripts shape emotion expression, interpersonal styles and moral judgments.

Interactionist perspective
Behaviour = f(person, environment). Kurt Lewin’s formula B = f(P, E) captures that both personal characteristics (genes, traits, beliefs) and situational context jointly determine behaviour. For many traits there is no single cause; rather, multiple factors contribute in differing proportions.

How psychologists study these bases
Common methods include case studies (e.g., Phineas Gage for frontal lobe function), twin & adoption studies (to estimate genetic vs environmental contributions), experiments (to test causal effects), neuroimaging & electrophysiology (fMRI, EEG) and correlational surveys. Each method has strengths and limits; converging evidence is used to draw reliable conclusions.

Practical implications
Understanding bases of behaviour helps in education (teaching methods matched to cognition), mental health (biopsychosocial approaches to treatment), public policy (nudges, social campaigns), and personal development (awareness of how stress, sleep, culture influence behaviour).

Summary
The bases of human behaviour are multifaceted—biological, psychological and socio‑cultural forces interact continuously. Psychology aims to describe these influences, explain mechanisms, predict outcomes and apply findings to improve wellbeing.

Fig 2 — Educational Diagram: Levels of analysis

Definition: "Levels of analysis" is the idea that human behaviour can be studied at different but interacting levels — biological, psychological (individual) and social (cultural/environmental). Each level provides a valid perspective; together they give a fuller explanation.

Three main levels:

1. Biological level
Focus: brain structures, neurotransmitters, hormones, genes, physiology. Explanations ask how bodily processes enable or predispose a behaviour. Methods include neuroimaging (fMRI, PET), EEG, genetic studies, endocrinology, pharmacology.

2. Psychological (individual) level
Focus: cognition (thoughts, attention, memory), emotions, learning, motivation, personality. Explanations analyse internal mental processes and behavioural learning histories. Methods include experiments, psychometric tests, reaction-time tasks, clinical interviews.

3. Social / Cultural level
Focus: family, peers, social roles, cultural norms, socioeconomic conditions, institutions. Explanations consider how social context shapes behaviour through modelling, reinforcement, expectations and opportunities. Methods include surveys, naturalistic observation, ethnography, cross-cultural comparisons.

How the levels interact
Behaviour often arises from interactions across levels. For example, genes may create a predisposition, cognitive appraisals trigger responses, and the social environment shapes whether a behaviour is expressed. Avoid strict reductionism (explaining everything only in one level) — integrate levels for complete explanations.

Types of cause and explanation: proximal (immediate mechanisms — e.g., hormone surge causing arousal) vs distal (longer-term causes — e.g., cultural norms, developmental history). Researchers use multi-method approaches and models (e.g., biopsychosocial) to combine evidence from levels.

Example application — Aggression (concise multi-level analysis):
• Biological: Higher testosterone, reduced prefrontal inhibition, or certain genetic variants may increase impulsive aggression.
• Psychological: Hostile attribution bias (thinking others intend harm), aggressive scripts learned via reinforcement, high anger and poor emotion regulation.
• Social: Exposure to violent media, family violence, peer reinforcement, poverty and social stressors increase likelihood of aggressive acts.

Implications for research and interventions
Choose methods matched to the level you investigate (e.g., EEG for neural timing, experiments for causal cognition, surveys for cultural patterns). Effective interventions often work across levels — e.g., medication or biofeedback (biological) + cognitive-behavioural therapy (psychological) + family/peer interventions (social).

Limitations and cautions
• Single-level explanations can be incomplete.
• Correlation vs causation: biological correlates do not always indicate causal mechanisms.
• Ethical concerns when using biological explanations (stigma, determinism).

Study tip: When given a behaviour, practise writing short multi-level analyses: 1–2 sentences per level + one interaction sentence.

Fig 3 — Educational Diagram: Structure and function of the nervous system

Overview
The nervous system is the body's rapid communication network. It receives sensory input, integrates information, and produces responses that maintain homeostasis and enable behaviour, learning and memory. It is divided into the Central Nervous System (CNS) and the Peripheral Nervous System (PNS).

Major divisions

CNS: Brain and spinal cord. Responsible for processing information, decision-making, higher mental functions and reflex coordination.
PNS: All neural tissue outside the CNS. Divided into the Somatic Nervous System (controls voluntary movements and sensory information) and the Autonomic Nervous System (ANS — controls involuntary functions). The ANS further divides into Sympathetic (fight-or-flight) and Parasympathetic (rest-and-digest) systems.

Neuron: structure and role

Neurons are the functional units of the nervous system. Key parts:

• Cell body (soma): contains nucleus and metabolic machinery.
• Dendrites: receive incoming signals (many, branched).
• Axon: long fibre that conducts impulses away from the soma. Ends in axon terminals/synaptic boutons.
• Myelin sheath: fatty insulation produced by Schwann cells (PNS) or oligodendrocytes (CNS); increases conduction speed. Nodes of Ranvier are gaps where ion exchange occurs.

Types of neurons

Sensory (afferent) neurons: carry information to CNS. Motor (efferent) neurons: carry commands to effectors (muscles/glands). Interneurons: link neurons within CNS and perform integration.

How signals are generated and transmitted

Resting membrane potential: a neuron's inside is negatively charged relative to outside (approx. −70 mV) due to ion distribution and selective membrane permeability maintained by Na+/K+ pumps.

Action potential (nerve impulse): a rapid, transient reversal of membrane potential that travels along the axon when threshold is reached. Sequence:

• Depolarization: voltage-gated Na+ channels open → Na+ influx → membrane potential becomes positive.
• Repolarization: Na+ channels inactivate, K+ channels open → K+ efflux → membrane returns toward negative.
• Hyperpolarization and refractory period: membrane briefly becomes more negative than resting; neuron cannot fire immediately again (absolute and relative refractory periods).

Saltatory conduction: In myelinated axons the action potential jumps between Nodes of Ranvier, greatly increasing conduction speed compared to continuous conduction in unmyelinated axons.

Synapses and transmission

Synapses are junctions between neurons. Chemical synapses: arrival of an action potential triggers neurotransmitter release (e.g., acetylcholine, dopamine, serotonin) into the synaptic cleft; neurotransmitters bind to receptors on the postsynaptic cell to excite or inhibit it. Electrical synapses allow direct ionic current flow via gap junctions (faster but less modifiable).

Reflexes

A reflex arc produces fast, automatic responses. Typical pathway: receptor → sensory neuron → (spinal) interneuron → motor neuron → effector. The knee-jerk (patellar) reflex is a monosynaptic reflex (no interneuron) producing immediate muscle contraction.

Functions of the nervous system

• Sensory detection and perception
• Integration and decision making (CNS)
• Motor control and coordination
• Autonomic regulation of internal organs (heart, digestion, respiration)
• Higher functions: language, reasoning, memory, emotion
• Plasticity: ability to change synaptic strength (basis of learning and memory)

Important notes for students

• Distinguish CNS vs PNS and somatic vs autonomic pathways.
• Be able to label a neuron and describe action potential phases.
• Understand how myelination and axon diameter affect conduction speed.
• Know a simple reflex arc and examples of sympathetic vs parasympathetic actions.

Fig 4 — Educational Diagram: Neurons and neural communication

What is a neuron? A neuron is a specialised nerve cell that receives, processes and transmits information by electrical and chemical signals. Each neuron has three main parts: dendrites (input), a cell body or soma (integration), and an axon (output). Many axons are wrapped in myelin sheaths with Nodes of Ranvier that speed conduction.

Types of neurons

• Sensory (afferent) neurons: carry information from sense organs to the CNS.
• Motor (efferent) neurons: carry commands from the CNS to muscles/glands.
• Interneurons: connect neurons within the CNS and perform integration.

Resting membrane potential: Neuron membranes maintain a resting potential (typically ≈ -70 mV) because of differences in ion concentrations (mainly Na+ and K+) and selective membrane permeability. The inside is negative relative to the outside.

How signals travel within a neuron — Action potential (electrical)

• When a stimulus depolarises the membrane to threshold (~ -55 mV), voltage-gated Na+ channels open → rapid Na+ influx → depolarisation.
• At the peak, Na+ channels inactivate and K+ channels open → K+ efflux → repolarisation.
• Often there is a brief hyperpolarisation (more negative than rest) before returning to resting potential.
• Absolute and relative refractory periods limit how soon another AP can occur and help determine firing rate.
• Myelinated axons conduct by saltatory conduction: APs jump between Nodes of Ranvier, greatly increasing speed.

How neurons communicate between cells — Synaptic (chemical) transmission

• Action potential arrives at axon terminal → voltage-gated Ca2+ channels open → Ca2+ enters terminal.
• Ca2+ triggers synaptic vesicles to fuse with the membrane and release neurotransmitter into the synaptic cleft.
• Neurotransmitter binds to receptors on the postsynaptic cell, causing ion channels to open or second-messenger changes.
• Postsynaptic responses: excitatory postsynaptic potentials (EPSPs) move membrane toward threshold; inhibitory postsynaptic potentials (IPSPs) move it away.
• Neurotransmitter action ends by reuptake, enzymatic breakdown, or diffusion.

Coding of information: Neurons code stimulus intensity by firing rate (frequency coding): stronger stimuli produce higher firing frequency. They also use spatial and temporal summation of EPSPs and IPSPs at the axon hillock to decide whether to fire an AP.

Plasticity and learning: Repeated activation can strengthen synapses (long-term potentiation) or weaken them (long-term depression). Synaptic changes underlie learning and memory.

Clinical and real-world relevance (brief): Loss of myelin (multiple sclerosis) slows conduction; Parkinson's disease results from loss of dopamine neurons; many psychiatric drugs act by altering synaptic neurotransmitter levels (e.g., SSRIs increase serotonin in the synapse).

Key takeaways

• Neurons transmit information electrically within and chemically between cells.
• Action potentials are all-or-none events; information about intensity is in frequency.
• Synaptic plasticity is the physiological basis for learning and memory.

Fig 5 — Educational Diagram: Brain: major divisions and functions

The brain is the central organ of the nervous system and can be described at several levels. Anatomically and functionally it is commonly divided into three major parts: forebrain, midbrain and hindbrain. Each major division contains substructures that perform specific roles in perception, action, emotion, cognition and homeostasis.

1. Forebrain (Prosencephalon)

• Telencephalon (Cerebral hemispheres)
  • Cerebral cortex: the outer folded layer responsible for higher mental functions. Divided into four lobes:
    • Frontal lobe – executive functions, planning, decision-making, voluntary movement (primary motor cortex), Broca’s area (speech production) on the left in most people.
    • Parietal lobe – somatosensory processing (primary somatosensory cortex), spatial attention, body schema.
    • Temporal lobe – auditory processing, memory-related structures; Wernicke’s area (language comprehension) typically on the left; hippocampus (memory formation) lies medially.
    • Occipital lobe – primary visual cortex and visual processing.
  • Basal ganglia: subcortical nuclei (caudate, putamen, globus pallidus) involved in movement initiation, habit formation and procedural learning.
  • Limbic system: set of structures (amygdala, hippocampus, cingulate cortex) important for emotion, motivation, and memory consolidation.
• Diencephalon
  • Thalamus – major relay station for sensory information (except olfaction) to the cortex; also involved in gating attention and sleep–wake regulation.
  • Hypothalamus – homeostasis (temperature, hunger, thirst), controls autonomic nervous system and endocrine system via the pituitary gland; links emotion with physiological states.

2. Midbrain (Mesencephalon)

• Acts as a conduit between forebrain and hindbrain and contains important nuclei and tracts.
• Superior and inferior colliculi – orienting movements of eyes/head to visual and auditory stimuli respectively.
• Substantia nigra – dopaminergic neurons important for movement; degeneration is linked to Parkinson’s disease.
• Involved in eye movements, auditory/visual reflexes and basic motor control.

3. Hindbrain (Rhombencephalon)

• Metencephalon
  • Cerebellum – coordination of voluntary movements, balance, motor learning and fine timing/precision. Important for smoothing actions and adapting movement based on feedback.
  • Pons – relays information between cortex and cerebellum, contains nuclei for sleep regulation, respiration modulation and cranial nerves.
• Myelencephalon
  • Medulla oblongata – vital autonomic centers for heart rate, blood pressure, breathing, swallowing and basic reflexes.

Other key functional concepts

• Localization of function: specific cortical areas are specialized (e.g., motor cortex, visual cortex, language areas), but many tasks require distributed networks and association areas that integrate information.
• Hemispheric lateralization: left hemisphere usually specializes in language and sequential processing; right hemisphere in spatial, holistic and nonverbal processing. Both hemispheres interact via the corpus callosum.
• Brainstem functions: integrates sensory and motor information for survival functions (breathing, heart rate), arousal and sleep–wake cycles (reticular formation).
• Neurochemical modulation: neurotransmitter systems (dopamine, serotonin, acetylcholine, norepinephrine) arising from subcortical nuclei modulate mood, attention, reward and arousal.
• Plasticity: the brain can reorganize following experience or injury (e.g., cortical remapping after training or damage), which underlies learning and rehabilitation.

Clinical/functional examples (summary)

• Stroke in a specific arterial territory (e.g., middle cerebral artery) can produce loss of movement and sensation in contralateral face/arm and language deficits if the dominant hemisphere is affected.
• Parkinson’s disease: degeneration of substantia nigra → reduced dopamine → resting tremor, rigidity, bradykinesia.
• Hippocampal damage → difficulty forming new episodic memories (anterograde amnesia).

Understanding major brain divisions helps connect structure to psychological functions: sensory processing, motor control, memory, emotion, language and homeostasis are supported by identifiable brain regions that interact as networks.

Fig 6 — Educational Diagram: Cerebral cortex and lobes

Overview
The cerebral cortex is the thin, folded outer layer of the cerebrum responsible for higher mental functions: perception, voluntary action, language, thinking and planning. It is composed mainly of gray matter (neuronal cell bodies) and is organized into layers and specialized regions (areas) that together support complex behaviour.

Structure

• Laminae (layers): The neocortex has six layers (I–VI) with different cell types and connectivity; layer V contains large projection neurons (e.g., Betz cells in motor cortex).
• Columnar organization: Neurons are also arranged in vertical columns that act as basic processing units.
• Brodmann areas: Cortex is divided into cytoarchitectonic areas (Brodmann areas) that correlate with functional specializations (e.g., BA17 = primary visual cortex).
• Gray vs white matter: Gray matter = neuronal cell bodies (cortex); white matter = myelinated axons linking cortical areas and other brain regions.

Lobes and principal functions

• Frontal lobe: Executive functions (planning, decision-making, inhibition), motor control (primary motor cortex, precentral gyrus), language production (Broca’s area, typically left hemisphere), working memory and personality (prefrontal cortex).
• Parietal lobe: Somatosensory processing (primary somatosensory cortex, postcentral gyrus), spatial attention and visuospatial integration, body awareness and tactile perception.
• Temporal lobe: Auditory processing (primary auditory cortex), language comprehension (Wernicke’s area, typically left), memory-related structures (medial temporal lobe — hippocampus), and high-level visual recognition (e.g., fusiform gyrus for faces).
• Occipital lobe: Primary visual cortex (V1) and visual association areas responsible for processing visual features (orientation, motion, colour) and constructing visual perception.

Association areas and integration
The majority of the cortex is association cortex (between primary sensory and primary motor areas). Association areas integrate multisensory information and support complex tasks such as language, problem solving, social cognition and planning.

Lateralization
Some functions show hemispheric specialization: for most right-handed people, left hemisphere is dominant for language production and logical reasoning, while the right is often stronger for spatial processing, face recognition and some aspects of emotion.

Plasticity and development
The cortex changes with experience (synaptic pruning, strengthening, and cortical reorganization). Developmental changes (childhood/adolescence) include synaptogenesis and later pruning; aging may involve cortical thinning in some regions.

Clinical relevance
Damage to specific cortical areas produces predictable deficits: lesions in primary motor cortex cause weakness/paresis, lesions in Broca’s area cause expressive aphasia, parietal lesions can cause neglect, occipital lesions can produce visual field defects, and temporal lobe pathology can impair memory or recognition.

Key concepts to remember

• Primary areas (sensory/motor) do basic processing; association areas integrate and interpret.
• Functional localization is approximate — many tasks require networks across lobes.
• Cortical maps (e.g., sensory and motor homunculi) show disproportionate representation according to usage and sensitivity.

Fig 7 — Educational Diagram: Localization and lateralization of function

Localization of function means that specific psychological functions (like language, vision, movement) are primarily served by particular, identifiable brain regions. Classic examples are the motor cortex for voluntary movement, the primary visual cortex for basic visual processing, Broca's area for speech production, and Wernicke's area for language comprehension.

Lateralization of function refers to the tendency for some functions to be more dominant in one cerebral hemisphere than the other. For most right-handed people, language tends to be left-hemisphere dominant, while spatial and face-processing abilities are often stronger in the right hemisphere.

Historical and research methods

• Key early findings: Broca (speech production) and Wernicke (language comprehension) demonstrated localization by studying patients with lesions.
• Methods used: lesion studies, electrical stimulation, split-brain (corpus callosum) research, Wada test, neuroimaging (fMRI, PET), EEG/ERP.

Major localized areas (brief)

• Primary motor cortex: voluntary movement control.
• Primary somatosensory cortex: touch, proprioception.
• Primary visual cortex (occipital lobe): initial visual processing.
• Auditory cortex (temporal lobe): sound processing.
• Broca's area (left inferior frontal gyrus): speech production; lesions cause nonfluent/agrammatic aphasia.
• Wernicke's area (left superior temporal gyrus): language comprehension; lesions cause fluent but nonsensical speech.

How lateralization shows up

• Language: typically left-dominant for grammar and speech in most people.
• Visuospatial tasks and face recognition: often right-dominant.
• Emotion and prosody: right hemisphere important for emotional tone of voice.
• Handedness relates but does not determine lateralization; left-handers show more variability.

Clinical implications

• Stroke in the middle cerebral artery territory of the left hemisphere often produces aphasia (language deficits), illustrating localization and lateralization.
• Right-hemisphere damage can cause hemispatial neglect (ignoring left side of space), showing both localization and lateralized function.

Key points and nuance

• Localization is not absolute: complex functions arise from networks; many areas interact.
• Lateralization is probabilistic and variable across individuals, sexes, and development.
• Plasticity: young brains can reorganize functions (e.g., language shifts after early injury).

Fig 8 — Educational Diagram: Brain plasticity and development

Definition: Brain plasticity (neuroplasticity) is the brain's ability to change its structure and function in response to experience, learning, and injury. Brain development refers to the sequential biological processes (neurogenesis, migration, differentiation, synaptogenesis, myelination and pruning) that shape the nervous system from prenatal stages through adulthood.

Major stages of brain development

• Neurogenesis: Generation of neurons (mainly prenatal; continues in limited regions like the hippocampus).
• Migration and differentiation: Neurons move to their positions and develop specific identities.
• Synaptogenesis: Rapid formation of synapses—especially intense in early childhood (sensory and motor areas first, prefrontal later).
• Myelination: Oligodendrocytes form myelin sheaths that speed neural transmission; continues into adolescence and early adulthood.
• Synaptic pruning: Elimination of excess synapses to increase efficiency—experience helps determine which synapses are retained.

Types of plasticity

• Structural plasticity: Physical changes such as dendritic branching, synapse formation, axon sprouting and cortical map reorganization.
• Functional plasticity: Changes in the strength or efficacy of synaptic transmission (e.g., long-term potentiation or depression).

Key principles

• “Use it or lose it”: Synapses and circuits that are used are strengthened; unused ones are pruned.
• Experience-expectant plasticity: The brain expects certain typical inputs (e.g., visual stimulation) during critical/sensitive periods to develop normally.
• Experience-dependent plasticity: Brain changes that occur from individual, unique experiences (e.g., learning an instrument).
• Critical and sensitive periods: Time windows when particular experiences have especially strong effects (language, binocular vision). Sensitivity declines but rarely goes to zero.
• Hebbian principle: Coordinated activity strengthens connections—often summarized as “cells that fire together, wire together.”

Plasticity across the lifespan

Plasticity is greatest in early development (high synaptogenesis and pruning), remains significant in childhood and adolescence (continued myelination and reorganization), and persists into adulthood (learning, recovery, adult neurogenesis in limited areas). Younger brains often recover better from injury because of greater reorganization capacity, though adults can form new skills and compensate.

Examples of mechanisms and outcomes

• Long-Term Potentiation (LTP): Repeated co-activation of synapses increases synaptic strength—cellular basis for learning and memory.
• Cortical reorganization: After limb amputation or sensory loss, neighbouring cortical areas can expand into the unused region (e.g., enhanced tactile representation in blind people).
• Environmental effects: Enriched environments (toys, social interaction) promote dendritic growth; deprivation can impair development.

Educational and clinical implications

• Early stimulation and varied experiences support optimal development (language exposure, play, social interaction).
• Interventions (rehabilitation, training) can harness plasticity after injury—timing and intensity matter.
• Understanding sensitive periods helps design age-appropriate learning strategies.

Limitations and cautions

Plasticity is not unlimited: biological constraints, age, severity of injury, and genetics influence the extent of change. ‘‘Sensitive’’ periods reduce but do not completely eliminate capacity for later change.

Fig 9 — Educational Diagram: Peripheral nervous system and autonomic nervous system

Overview: The peripheral nervous system (PNS) is the part of the nervous system outside the brain and spinal cord (CNS). It connects the CNS to muscles, glands and sensory receptors. The PNS is divided into sensory (afferent) and motor (efferent) pathways. The motor (efferent) division further splits into the somatic nervous system (voluntary control of skeletal muscles) and the autonomic nervous system (ANS), which controls involuntary functions (heart, digestion, glands, smooth muscle).

Structure and divisions:

• Peripheral nervous system: 12 pairs of cranial nerves + 31 pairs of spinal nerves; sensory (to CNS) and motor (from CNS) fibers.
• Somatic nervous system: Motor neurons that innervate skeletal muscle; usually single neuron from CNS to effector; voluntary and consciously controlled.
• Autonomic nervous system (ANS): Regulates internal organs and homeostasis; mostly involuntary. Divided into sympathetic, parasympathetic and enteric divisions.

Autonomic nervous system — key features:

• Sympathetic division: "Fight-or-flight". Prepares body for stress or activity. Typical effects: increases heart rate and blood pressure, dilates pupils, dilates bronchi, inhibits digestion, mobilizes glucose.
• Parasympathetic division: "Rest-and-digest". Conserves energy and supports digestion. Typical effects: decreases heart rate, constricts pupils, stimulates digestion, promotes glandular secretion.
• Enteric nervous system: Network of neurons in the gastrointestinal tract that can operate independently but is modulated by sympathetic and parasympathetic inputs.

Anatomical and chemical differences:

• Preganglionic neurons originate in CNS and synapse in autonomic ganglia. Postganglionic neurons go from ganglia to target organs.
• Sympathetic ganglia: close to spinal cord (paravertebral chain). Parasympathetic ganglia: near or within target organs.
• Neurotransmitters: Preganglionic neurons (both divisions) release acetylcholine (ACh). Parasympathetic postganglionic neurons release ACh. Sympathetic postganglionic neurons usually release norepinephrine (noradrenaline). Exceptions: sympathetic innervation of sweat glands uses ACh; adrenal medulla releases epinephrine and norepinephrine into blood.

Functional examples and reflexes:

• Reflex arc (simple formula-like sequence): Stimulus → Receptor → Sensory (afferent) neuron → Interneuron (in spinal cord) → Motor (efferent) neuron → Effector → Response. Example: knee-jerk (monosynaptic) and withdrawal reflex (polysynaptic).
• Somatic actions are voluntary (e.g., picking up a book). Autonomic actions are automatic (e.g., heartbeat, digestion, pupil size).

Physiology basics:

• Neurons conduct electrical impulses (action potentials). Typical values: resting membrane potential ≈ −70 mV; threshold ≈ −50 to −55 mV; action potential peak ≈ +30 mV.
• Conduction is faster in myelinated fibers and in axons with larger diameter. Myelin enables saltatory conduction (impulse jumps between nodes of Ranvier).

Clinical relevance:

• Autonomic dysfunction can cause orthostatic hypotension (blood pressure drop on standing), abnormal sweating, or gastroparesis (slow gastric emptying).
• Drugs that affect ANS: beta-blockers (reduce sympathetic heart stimulation), anticholinergics (block parasympathetic ACh receptors), sympathomimetics (mimic sympathetic activity), cholinomimetics (mimic parasympathetic activity).

Summary: The PNS transmits information between the body and the CNS. The somatic system controls voluntary movements; the autonomic system controls involuntary internal functions through a balance of sympathetic (arousing) and parasympathetic (calming) activities.

Fig 10 — Educational Diagram: Endocrine system and hormones

Overview: The endocrine system is a network of glands that secrete chemical messengers called hormones into the bloodstream. Hormones regulate physiology and behaviour — metabolism, growth, sleep, mood, stress responses, reproduction and development.

Main glands and key hormones (and behavioural effects):

• Hypothalamus: releasing and inhibiting hormones that control the pituitary; links brain and endocrine system (affects appetite, stress and sleep).
• Pituitary (master gland): anterior pituitary secretes GH (growth, sleep-related behaviour), ACTH (stimulates cortisol — stress), TSH (stimulates thyroid — energy, mood), FSH/LH (reproduction, sexual development); posterior pituitary releases oxytocin (bonding, childbirth) and vasopressin/ADH (water balance, social behaviour).
• Thyroid: T3/T4 — regulate basal metabolic rate, energy levels, attention, mood. (Hyperthyroidism can cause anxiety, hypo causes lethargy).
• Adrenal glands: cortisol (stress hormone — attention, memory modulation), adrenaline/noradrenaline (fight-or-flight — arousal, heart rate, alertness).
• Pancreas: insulin and glucagon regulate blood glucose; important for energy availability and cognitive performance.
• Gonads (ovaries/testes): estrogen, progesterone, testosterone — influence sexual development, motivation, aggression, mood and social behaviour.
• Pineal gland: melatonin — circadian rhythms and sleep-wake cycles.

Chemical nature and mechanism of action:

• Types of hormones: peptides/proteins (e.g., insulin), steroids (e.g., cortisol, testosterone), and amines (e.g., adrenaline, thyroid hormones).
• Action mechanisms: Peptide hormones bind to cell-surface receptors and use second-messenger systems (fast effects). Steroid and thyroid hormones are lipid-soluble and bind intracellular receptors to change gene transcription (slower but long-lasting effects).

Control and feedback: Most endocrine axes use negative feedback. Example: hypothalamus → TRH → pituitary → TSH → thyroid → T3/T4. High T3/T4 suppress TRH/TSH release. Feedback maintains homeostasis and stabilizes behaviour (e.g., energy balance).

Link to behaviour: Hormones modulate arousal, emotion, cognition and development. Examples: cortisol modulates attention and memory during stress; adrenaline increases vigilance and reaction speed; oxytocin promotes trust and bonding; sex hormones shape pubertal changes in identity, motivation and risk-taking.

Common disorders and behavioural signs:

• Diabetes mellitus: insulin deficiency/resistance — fatigue, poor concentration, mood changes.
• Hypothyroidism: low T3/T4 — lethargy, depression, slow thinking.
• Hyperthyroidism: high T3/T4 — anxiety, irritability, restlessness.
• Cushing's syndrome: chronic high cortisol — memory problems, mood swings, fatigue.
• Addison's disease: low adrenal hormones — weakness, apathy, mood changes.

Practical classroom points: Understand glands, major hormones and their behavioural effects; know negative feedback; use examples (stress, sleep, puberty). Many effects are modulatory — hormones change probability of behaviours rather than directly causing specific actions.

Fig 11 — Educational Diagram: Genetics: basic concepts

Overview: Genetics is the study of how biological traits are passed from parents to offspring. In psychology, genetics helps explain individual differences in behaviour, temperament, abilities and susceptibility to mental disorders.

Basic units: A gene is a segment of DNA that codes for a trait. Different forms of a gene are called alleles. Genes are located on chromosomes (humans have 23 pairs). The full genetic makeup of an organism is its genotype, while the observable characteristics constitute its phenotype.

Mendelian inheritance: Gregor Mendel described two key principles: the law of segregation (paired alleles separate during gamete formation so an offspring receives one allele from each parent) and the law of independent assortment (different gene pairs segregate independently). Traits can be dominant (expressed when at least one dominant allele present) or recessive (expressed only if two recessive alleles present). Variations include incomplete dominance (intermediate phenotype) and codominance (both alleles expressed).

Beyond simple Mendel: Many psychological and physical traits are polygenic (influenced by many genes) and show a continuous distribution (eg height, intelligence). Some traits are sex-linked (carried on X or Y chromosome) and some arise from mutations or chromosomal abnormalities (eg Down syndrome is trisomy 21).

Genes and environment: Phenotype results from both genes and environment. Simple decomposition is Vp = Vg + Ve, where Vp is phenotypic variance, Vg genetic variance and Ve environmental variance. Interaction and correlation between genes and environment are important: environment can modify gene expression (epigenetics), and genes can influence the environments people select. Examples include phenylketonuria (PKU) where dietary control prevents cognitive impairment despite genetic risk.

Heritability and methods: Heritability quantifies the proportion of phenotypic variance in a population attributable to genetic differences. It ranges from 0 to 1 (or 0% to 100%). Twin and adoption studies are common methods: monozygotic (MZ) twins share ~100% genes; dizygotic (DZ) twins share ~50% on average. Higher concordance or correlation in MZ than DZ twins suggests genetic influence.

Limitations: Heritability applies to populations, not individuals, and depends on the environment studied. High heritability does not mean immutability. Also many behaviours are multifactorial (many genes plus environment).

Fig 12 — Educational Diagram: Behavior genetics methods

Overview

Behavior genetics studies how genes and environment influence behavior and psychological traits. Methods try to separate genetic and environmental contributions by comparing relatives who differ in genetic relatedness and/or rearing environment.

Main methods

• Family (pedigree) studies: Examine whether a trait runs in families. Greater similarity among close relatives suggests genetic influence, but shared family environment can confound results.
• Twin studies: Compare monozygotic (MZ, identical) twins who share ~100% of genes with dizygotic (DZ, fraternal) twins who share ~50% of segregating genes. If MZ similarity > DZ similarity, genetics likely contributes. Twins reared apart help separate genes from shared environment.
• Adoption studies: Compare adopted children to their biological (genetic) vs adoptive (rearing) parents. Greater resemblance to biological parents indicates genetic influence; resemblance to adoptive parents indicates environmental influence.
• Selective breeding / animal studies: Breeding animals for high vs low trait values to show heredity of traits (used historically for behaviors and physiological traits).
• Molecular genetics approaches: Modern methods identify specific genes or variants (candidate gene studies, linkage analysis, GWAS) associated with traits.

Key concepts

• Concordance: Proportion of pairs in which both relatives show a trait (commonly used in twin studies for categorical traits).
• Correlation / similarity: For continuous traits (e.g., IQ, height), use correlation coefficients between relatives.
• Heritability (broad sense / narrow sense): Proportion of observed variance in a trait attributable to genetic differences in a population. Heritability is population- and environment-specific and does not apply to individuals.
• Shared vs non-shared environment: Shared environment makes relatives similar (family influences); non-shared environment makes them different (unique experiences).
• Gene × Environment interaction & correlation: Genes can influence sensitivity to environments (G×E), and genes can influence the probability of experiencing certain environments (rGE).

Assumptions and limitations

• Equal environments assumption (EEA) for twin studies: assumes MZ and DZ twins experience equally similar environments — if false, genetic influence may be overestimated.
• Heritability does not imply immutability: high heritability does not mean a trait cannot be changed by environment.
• Population-specific: heritability estimates change across populations, ages, and environments.

How results are interpreted

• Compare resemblance: e.g., if MZ concordance far greater than DZ, strong genetic influence; if MZ and DZ roughly equal, shared environment is important.
• Use formulas (below) to estimate genetic and environmental variance components.

Summary: Behavior genetics uses family, twin, adoption, breeding and molecular methods to estimate genetic and environmental contributions to behavior. Results give population-level estimates (heritability, shared/non-shared environment) and are interpreted cautiously because of assumptions and gene–environment interplay.

Fig 13 — Educational Diagram: Gene–environment interaction and correlation

Overview

Behaviour is shaped by both genes (G) and environments (E). Two related but distinct concepts explain how genes and environments jointly influence traits: gene–environment interaction (G×E) and gene–environment correlation (rGE).

Gene–environment interaction (G×E)

G×E occurs when the effect of a person’s genotype on a trait depends on the environment, or when an environmental effect depends on genotype. In other words, the same environment does not affect everyone equally, and the same genotype does not produce the same outcome in all environments. Models used to describe G×E include diathesis–stress (genetic vulnerability expressed under stress) and differential susceptibility (some genotypes are more sensitive to both negative and positive environments).

Gene–environment correlation (rGE)

rGE occurs when genetic factors influence the likelihood of exposure to particular environments. There are three types:

• Passive rGE: Biological parents provide both genes and the rearing environment (e.g., musical parents pass on genes for musical ability and create a music-rich home).
• Evocative (reactive) rGE: A person's genetically influenced traits evoke certain responses from others (e.g., a sociable child elicits more social interaction from peers and adults).
• Active rGE: Individuals select or create environments that match their genetic tendencies (e.g., a person with athletic aptitude chooses sports and training).

Why it matters

Understanding G×E and rGE helps explain individual differences, why people with similar genes differ across contexts, and why environmental interventions may work better for some people than others. These concepts are central to developmental, clinical and educational psychology, and to policies that aim to change environments (e.g., early education, nutrition).

How researchers study them

Common methods include twin and adoption studies (to separate genetic and environmental variance), longitudinal studies, and molecular methods that test specific gene–environment interactions. Interpretation requires care because correlations between genes and environment can confound causal claims about environment effects.

Fig 14 — Educational Diagram: Evolutionary influences on behaviour

What it is: Evolutionary influences on behaviour refers to how natural selection and related evolutionary processes shape psychological mechanisms and behavioural tendencies that increased the chances of survival and reproduction in our ancestors. These evolved mechanisms are called evolved psychological mechanisms (EPMs).

Core principles

- Variation: Individuals differ in traits and behaviours.
- Heritability: Some behavioural tendencies have a genetic basis and can be passed to offspring.
- Differential reproductive success: Traits that increased survival or mating success tend to become more common.

Key concepts and applications

- Natural selection: Behaviours that improved survival (e.g., avoiding predators) or reproduction (e.g., attracting mates) were favoured.
- Sexual selection: Traits that improve mating success (mate preferences, displays, competition) evolve even if they carry some survival cost.
- Instincts and fixed action patterns: Innate response sequences (e.g., baby grasping) evolved because they increased early survival. Konrad Lorenz and ethologists described many such patterns.

- Kin selection and inclusive fitness: Helping genetically related individuals can increase the helper’s inclusive fitness (own reproduction + effects on relatives). Hamilton formalised this.

- Reciprocal altruism: Cooperation between non-relatives can evolve if individuals help others with expectation of future return (tit-for-tat dynamics).

- Parental investment theory: The sex that invests more in offspring (usually females) becomes choosier about mates; the lower-investing sex competes more for access to mates (Trivers).

- Universal emotions and communication: Some facial expressions and emotional responses are cross-cultural and presumed to be evolved signalling systems (Darwin, Ekman).

- Evolutionary mismatch: Behavioural tendencies adapted for ancestral environments (e.g., craving calorie-dense foods) can be maladaptive in modern contexts (obesity, phobias to harmless stimuli).

Important contributors: Charles Darwin (natural selection), Konrad Lorenz and Nikolaas Tinbergen (ethology), W. D. Hamilton (kin selection), Robert Trivers (parental investment & reciprocity), John Bowlby (attachment theory—an ethological/evolutionary approach).

Limitations and cautions

- Evolutionary explanations are often probabilistic and historical; they do not imply behaviours are genetically fixed.
- Many behaviours result from gene–environment interaction.
- Avoid just-so stories: hypotheses should be testable and supported by evidence (comparative data, cross-cultural studies, developmental and genetic research).

Fig 15 — Educational Diagram: Cultural and environmental influences

Definition: Cultural and environmental influences are external forces that shape human behaviour, thoughts, emotions and development. 'Culture' refers to the shared values, beliefs, norms, symbols and practices of a group. 'Environment' includes the social, physical and economic surroundings in which a person lives.

How culture influences behaviour

• Content of culture: values, norms, language, religion, customs and artefacts provide frameworks for interpretation and action.
• Socialisation: From infancy people learn culturally approved behaviours by imitation, instruction, reinforcement and participation (family, school, peers, media).
• Roles and expectations: Culture defines social roles (gender, age, occupational) and situational norms that guide behaviour and choices.
• Cognitive and emotional patterns: Culture shapes attention, perception, reasoning styles (e.g., holistic vs analytic), display rules for emotion, and moral judgments.

How environment influences behaviour

• Physical environment: climate, housing, crowding, noise, pollution and access to resources affect health, stress, sleep, and cognitive functioning.
• Socioeconomic context: Family income, education, occupation and neighbourhood safety influence opportunities, stress exposure and developmental outcomes.
• Biological prenatal/early environment: Nutrition, toxin exposure, maternal stress and stimulation shape brain development and later behaviour.
• Immediate social environment: parenting style, peer groups, teachers and community provide reinforcement, models and constraints for behaviour.

Key theoretical perspectives

• Lewin's field theory: Behaviour is a function of the person and their environment: B = f(P, E). This emphasises context and interacting influences.
• Bronfenbrenner's ecological systems: Development occurs within nested systems: microsystem (family, school), mesosystem (connections among microsystems), exosystem (parents' workplaces, media), macrosystem (culture, laws), chronosystem (time/history).
• Gene–environment interaction: Genes set potentials while environment can activate, suppress or modify expression; sensitive periods (early childhood) show higher plasticity.

Processes linking culture and environment to behaviour

• Enculturation: learning one’s own culture across development.
• Acculturation: cultural change that occurs when groups come into prolonged contact (e.g., immigrants adapting to a new culture).
• Social learning: modelling and reinforcement transmit cultural norms and practices.

Implications

• Behavioural norms, mental health expressions and attitudes vary across cultures; psychological theories must consider cultural context to avoid bias.
• Interventions (education, health, policy) are more effective when tailored to cultural and environmental realities (e.g., community resources, language, beliefs).

Short summary: Cultural and environmental influences interact with biological factors to produce observed human behaviour. Culture supplies meanings and rules; environment provides material conditions and social contexts. Together they shape development across the lifespan.

Fig 16 — Educational Diagram: Methods for studying the brain and behaviour

Introduction
Psychology links brain processes to behaviour. To study this link scientists use several methods — observational, electrical, stimulation, structural imaging and functional imaging — each giving different kinds of information (where, when and how brain activity relates to behaviour).

1. Clinical (lesion / case) studies

• Study people with brain damage (natural lesions from injury, stroke or surgery). Compare deficits to intact functions to infer brain–behaviour relationships (e.g., damage to hippocampus → memory problems).
• Strengths: strong causal inference when a function is lost; rich, detailed data. Weaknesses: lesions are rarely clean or confined; individual differences limit generalisation.

2. Neuropsychological tests and behavioural measures

• Standardised tests (memory tests, attention tests, intelligence tests), reaction-time tasks, observational checklists and questionnaires measure behaviour quantitatively.
• Used together with brain methods to relate scores to brain structure/function (e.g., low verbal memory score linked with temporal-lobe damage).

3. Electrical methods: EEG and ERPs

• EEG (electroencephalogram) records summed electrical activity from scalp electrodes. Good temporal resolution (milliseconds) but poor spatial resolution.
• ERP (event-related potential) is the averaged EEG response time-locked to a stimulus — useful for studying timing of perception, attention and decision processes.
• Used clinically (e.g., epilepsy diagnosis) and in research on attention, sleep, language.

4. Brain stimulation and single-cell recording

• Single-unit recording (mainly in animals) measures action potentials of individual neurons — excellent spatial and temporal precision.
• TMS (transcranial magnetic stimulation) non-invasively stimulates or temporarily disrupts a cortical area to test its causal role in behaviour (e.g., transiently disrupt motor cortex to study movement).
• Limitations: invasiveness (single-unit), limited depth and focality (TMS).

5. Structural imaging: CT and MRI

• CT (computed tomography) uses X-rays to show gross brain structure; fast, useful for detecting bleeding or major damage.
• MRI (magnetic resonance imaging) uses magnetic fields for high-resolution images of brain anatomy (grey & white matter, lesions).
• These show where structural damage or differences are located but do not measure real-time brain activity.

6. Functional imaging: PET and fMRI

• PET (positron emission tomography) uses radioactive tracers (e.g., glucose analog) to measure metabolic activity — shows active regions during tasks but has lower temporal resolution and involves radioactivity.
• fMRI (functional MRI) measures BOLD (blood-oxygen-level-dependent) signal related to neural activity — good spatial resolution and reasonable temporal resolution. Widely used to map brain activation during tasks (language, memory, emotion).
• Both allow correlating brain activation patterns with behavioural performance.

7. Combining methods and ethical issues

• Combining methods (e.g., EEG + fMRI, neuropsychological tests + structural MRI) gives complementary information: when (EEG) and where (fMRI/MRI).
• Ethical considerations: informed consent, minimizing harm (especially for invasive methods), safe use of radiation and magnetic fields, protecting privacy of brain data.

How methods answer different questions
- Causal vs correlational: lesion and stimulation methods can show causality; EEG, fMRI and PET are mostly correlational.
- Temporal resolution: EEG/ERP & single-unit > fMRI/PET.
- Spatial resolution: single-unit & fMRI/MRI > EEG/ERP.

Summary
Different methods provide different windows on the brain–behaviour link. Choice of method depends on the question (where vs when vs cause), the population (human vs animal), and ethical/practical constraints.

Fig 17 — Educational Diagram: Applications and implications

Overview
"Applications and implications" refers to how knowledge of the bases of human behaviour (biological, cognitive, developmental and socio‑cultural) is used in real life and what social, ethical and practical consequences follow. This covers applied fields (healthcare, education, workplace, law, marketing, technology) and broader implications (policy, ethics, stigma, reductionism, privacy).

Major application areas

• Mental health and clinical practice: Biological and cognitive insights guide diagnosis and treatment — e.g., psychopharmacology (neurochemical targets), cognitive‑behavioural therapy (restructuring maladaptive thoughts), neurofeedback and rehabilitation after brain injury.
• Education: Understanding development, learning mechanisms and individual differences leads to differentiated instruction, remediation for learning disorders (dyslexia, ADHD), and use of spaced practice, retrieval practice and multimodal teaching based on cognitive principles.
• Workplace and organizational settings: Application of motivation theories, ergonomics, job design, selection and training using psychometric tests, and stress management programs informed by biopsychosocial models.
• Legal and forensic uses: Knowledge about memory, eyewitness reliability, and mental state informs interrogation, witness assessment, and assessments of criminal responsibility; neuroscientific evidence may be used (with caution) in courts.
• Health promotion and public policy: Behaviour change interventions (smoking cessation, vaccination uptake) use social‑cognitive models and understanding of habit formation; policy designs (nudges) exploit cognitive biases to improve public outcomes.
• Technology and design: Human–computer interaction, user experience, brain–computer interfaces, and adaptive learning systems use cognitive and neurobiological principles to improve usability and accessibility.
• Marketing and media: Consumer behaviour research uses perception, emotion, and social influence findings to design messages, advertising strategies and product placement.

Key implications and cautions

• Ethical concerns: Privacy of neural and psychological data (e.g., neuroimaging, biometric tracking), informed consent, potential misuse (neuromarketing, surveillance), and fairness in selection tools.
• Reductionism vs. holism: Biological explanations are powerful but incomplete; behaviour arises from interactions between biology, cognition and environment. Overemphasis on one base can lead to flawed interventions.
• Determinism and stigma: Biological explanations for behaviour can reduce blame but may increase fatalism or stigma (e.g., labeling mental illness as immutable). Balanced communication is needed.
• Validity and reliability limits: Psychometric tools and neuroimaging have measurement limits; findings must be replicated and interpreted cautiously when applied to individuals.
• Social and policy consequences: Scientific findings can shape education systems, health funding, workplace laws and criminal justice — policies must weigh benefits, risks and equity.
• Interdisciplinary approach: Effective application usually requires combining biological, cognitive, social and developmental perspectives (e.g., biopsychosocial model in medicine).

Practical steps for applying knowledge responsibly

• Use evidence‑based interventions and monitor outcomes.
• Consider individual differences and cultural context.
• Ensure informed consent and protect sensitive data.
• Avoid overgeneralization from group data to individuals.
• Engage stakeholders (patients, students, employees) when designing interventions.

Summary
Knowledge of the bases of human behaviour has wide and valuable applications across health, education, law, work and society. However, every application carries ethical, methodological and social implications—responsible use requires critical interpretation, interdisciplinary thinking and protection of individual rights.