Biopsychology Chapter 3 Notes
3.1 Human Genetics
Learning objectives
Explain the basic principles of the theory of evolution by natural selection.
Describe the differences between genotype and phenotype.
Discuss how gene–environment interactions are critical for expression of physical and psychological characteristics.
Overview: psychology and genetics
Psychological researchers study genetics to understand biological factors contributing to behavior.
Humans share core biological mechanisms (brains, hormones, cells with DNA), but expression leads to diverse traits and behaviors.
Questions motivating the section: variable outcomes of disease, genetic diseases across families, genetic components of mental disorders, links to physical health (e.g., obesity).
Sickle-cell anemia as a paradigmatic case
Sickle-cell anemia: genetic disorder; red blood cells become crescent-shaped, impairing blood flow and causing fever, pain, swelling, tissue damage.
Two sisters example: Luwi (carrier, one sickle-cell gene) vs Sena (non-carrier).
Carriers experience malaria resistance in malaria-endemic areas due to altered blood chemistry/immune function; two copies (homozygous) do not provide malaria protection and cause disease.
Malaria interaction with sickle-cell trait illustrates natural selection in humans: a mutation that is detrimental in one environment can be advantageous in another (Darwinian fitness).
In regions with malaria, sickle-cell trait is relatively common among people of African descent because carriers have a survival advantage.
In malaria-free regions (e.g., United States), the gene offers little benefit and may have costs for carriers.
Link to learning: sickle cell mutation and malaria – mutation leads to variable fitness depending on environment.
Darwin’s theory and human genetics (Figure 3.3 overview)
Natural selection: better adaptation to environment increases survival and reproduction.
Example: carrier Luwi’s mutation is adaptive in Africa but could be costly elsewhere.
Genetic variation: origin and terminology
Humans start with a gamete fusion process: egg + sperm.
Egg and sperm each contain 23 chromosomes; fusion yields a zygote with 46 chromosomes (23 pairs).
Chromosomes carry deoxyribonucleic acid (DNA).
DNA is a helix-shaped molecule composed of nucleotide base pairs.
Genes are sequences of DNA that control or partially control traits (eye color, hair color, etc.).
Alleles are different versions of a gene.
Genotype vs. phenotype
Genotype: genetic makeup (DNA) inherited from parents.
Phenotype: observable characteristics resulting from gene–environment interaction.
The interaction of genotype and environment shapes phenotype (Fig. 3.4).
Single-gene vs. polygenic traits (Punnett squares and inheritance concepts)
Some traits are governed by a single gene; others are polygenic (many genes contribute).
Example: cleft chin is influenced by a single gene with two alleles (dominant B, recessive b).
In a cross between a cleft-chin mother (BB) and a smooth-chin father (bb), offspring are all Bb (cleft chin).
If the mother is Bb (heterozygous) and the father is bb (homozygous recessive), offspring have a 50% chance of cleft chin and 50% chance of smooth chin (Figure 3.5).
Sickle-cell, PKU, and genetics of disease
Heterozygous carriers for sickle-cell (one sickle gene) show malaria resistance; homozygous (two copies) have a severe disease without malaria protection.
PKU (phenylketonuria) is a recessive disorder caused by lack of an enzyme to convert harmful amino acids; requires both parents to carry the recessive allele; cross example in Fig. 3.6 shows 25% chance of PKU when both parents are heterozygous.
Polygenic traits
Most human traits are polygenic (e.g., height, skin color, weight).
Mutations and genetic variation
Mutations: sudden, permanent changes in genes; can be harmful or occasionally beneficial, providing variations that may aid adaptation.
Variability in genes enables populations to adapt to changing environments via natural selection.
Dig Deep: Human Diversity
Race as a variable in genetic research is controversial; after the human genome sequencing, many argue race is a weak construct for biology because more variation occurs within racial categories than between them.
Ancestry, rather than race, may be a more informative way to study genetic diversity and disease risk.
Gene–environment interactions: three perspectives
Range of reaction: genes set bounds on potential, environment determines where within that range a person falls; environment can influence expression within genetic potential.
Genetic–environmental correlation: genes influence the environment, and the environment influences gene expression (bidirectional equation in Fig. 3.7).
Epigenetics: environment can alter gene expression without changing the genotype; same genotype can yield different phenotypes due to epigenetic mechanisms.
Identical twins share DNA, but can show different phenotypes due to environmental influences and epigenetic changes; some diseases can manifest differently across twins.
Epigenetics and twin studies (Figure 3.7; linked content)
Epigenetics studies how identical genotypes can yield different phenotypes due to gene expression regulation across life.
Twin studies illustrate how genetic similarity interacts with divergent environments to produce different outcomes.
Gene–environment findings in mental health and behavior
Genes link to a range of traits including temperament, sexual orientation, spirituality, and susceptibility to disorders such as depression or schizophrenia.
A classic study (Tienari et al., 2004) on adoptees showed strong genetic risk (biological mother with schizophrenia) plus a disturbed environment led to higher schizophrenia risk (36.8%) than either high genetic risk with healthy environment (5.8%), low genetic risk with disturbed environment (5.3%), or low genetic risk with healthy environment (4.8%).
Key terms for 3.1
allele, epigenetics, genotype, phenotype, polygenic, mutation, PKU, sickle-cell anemia, natural selection, race, range of reaction, epigenetics, th
3.2 Cells of the Nervous System
Neurons and glia
Two main cell types: glial cells (glia) and neurons.
Glia provide support (physical/metabolic), insulation, nutrient/waste transport, immune mediation; historically thought to outnumber neurons, but recent research suggests a near 1:1 ratio with neurons (Azevedo et al., Herculano-Houzel work).
Neurons are the functional information processors.
Neuron structure (Figure 3.8)
Soma (cell body): contains nucleus.
Dendrites: input sites that receive signals from other neurons.
Axon: transmits signals away from the soma; ends in terminal buttons with synaptic vesicles containing neurotransmitters.
Myelin sheath: fatty insulation around many axons; speeds signal transmission; gaps are Nodes of Ranvier.
Nodes of Ranvier: gaps in myelin that facilitate rapid signal propagation (saltatory conduction).
Myelin and disease
PKU can reduce myelin; MS involves widespread demyelination; both disrupt neural signaling and cognitive/motor function.
Neuronal communication: synapse and neurotransmitters
Action potential travels along the axon to terminal buttons; synaptic vesicles release neurotransmitters into the synaptic cleft.
Neurotransmitters bind to receptors on the postsynaptic neuron via lock-and-key specificity.
Receptors match specific neurotransmitters; a given transmitter binds to any receptor that fits.
Resting potential and action potential (Figure 3.10, 3.11)
Neuron membranes maintain a resting potential: ions create a charge difference across the membrane.
Resting state: Na+ higher outside; K+ higher inside; inside is negative relative to outside.
Resting potential is maintained by ion gradients and the sodium–potassium pump.
When signals arrive at dendrites, ion channels open; Na+ influx depolarizes the cell toward threshold.
If threshold of excitation is reached, the action potential is triggered.
Depolarization: rapid Na+ influx; repolarization: K+ efflux; hyperpolarization then returns to resting potential.
Action potential is all-or-none: either reaches threshold and triggers a full spike or not; propagates with full strength along the axon (saltatory conduction in myelinated fibers).
Synaptic clearing and electrical vs chemical synapses
After neurotransmitter release, they are cleared via reuptake, enzyme breakdown, or diffusion.
Reuptake: neurotransmitter pumped back into the presynaptic neuron; helps reset the synapse and regulate transmitter production.
Electrical synapses (gap junctions) exist but are rarer and faster than chemical synapses.
Neurotransmitters and drugs (Table 3.1)
Major neurotransmitters and roles include:
Acetylcholine: muscle action; memory; arousal, cognition.
Dopamine: mood, sleep, learning; pleasure; appetite.
Norepinephrine: arousal, alertness; heart/intestines.
Serotonin: mood and sleep; appetite.
GABA (Gamma-aminobutyric acid): inhibitory; reduces anxiety.
Glutamate: memory, learning; primary excitatory.
Beta-endorphin: pain relief and pleasure.
Psychoactive drugs can act as agonists or antagonists:
Agonists: mimic or strengthen neurotransmitter effects at receptors.
Antagonists: block neurotransmitter activity at receptors.
Reuptake inhibitors (e.g., SSRIs) increase neurotransmitter activity by preventing reabsorption.
Examples:
Parkinson’s disease: low dopamine; treatment with dopamine agonists.
Schizophrenia: often treated with dopamine antagonists to reduce overactivity at dopamine receptors.
Depression: SSRIs (e.g., Prozac, Paxil, Zoloft) inhibit serotonin reuptake to increase serotonin signaling.
LSD: interacts with serotonin receptors similarly.
Drug treatment caveats: delayed onset of effects, side effects, individual variability; often combined with psychotherapy.
3.3 Parts of the Nervous System
CNS vs PNS
Central nervous system (CNS): brain and spinal cord.
Peripheral nervous system (PNS): nerves connecting CNS to body; carries sensory and motor information.
PNS subdivisions
Somatic nervous system: voluntary control; transmits sensory and motor information; consists of sensory (afferent) and motor (efferent) neurons.
Autonomic nervous system: regulates internal organs and glands; usually involuntary; subdivided into:
Sympathetic nervous system: prepares body for stress-related activities (fight or flight); broad activation of body systems.
Parasympathetic nervous system: returns body to baseline; resting functions (homeostasis).
Homeostasis: balance of biological states (e.g., body temperature) maintained through autonomic activity.
Quick reference (Figure 3.14)
Sympathetic vs. parasympathetic actions on pupil, salivation, heart rate, bronchi, digestion, bladder, etc.
3.4 The Brain and Spinal Cord
The spinal cord
Connects brain to the body; acts as a relay and reflex center.
30 spinal segments correspond to vertebrae; each segment connects to a body region via nerves.
Sensory nerves bring messages in; motor nerves send messages out.
Spinal reflexes: quick automatic responses (e.g., withdrawal from heat, knee-jerk).
Protective structures: vertebrae and cerebrospinal fluid.
Spinal injuries can cause paralysis below the injury level.
Neuroplasticity
The nervous system’s ability to change and adapt in response to experiences or injury.
Mechanisms: synapse formation/pruning, glial changes, neurogenesis in some regions.
Example: Bob Woodruff’s recovery from brain injury demonstrates plasticity and rehabilitation potential.
The two hemispheres and lateralization
Cerebral cortex surface shows gyri (ridges) and sulci (grooves); major landmark: longitudinal fissure, separating left and right hemispheres.
Lateralization: specialization of each hemisphere for certain functions; left often associated with language and memory associations; right with pitch, arousal, and negative emotions; however, results are not universal; hemispheres interact for most tasks.
Corpus callosum connects hemispheres (~200 million axons); enables interhemispheric communication.
Split-brain cases (severed corpus callosum) reveal how each hemisphere can support different functions and how information processed in one side can sometimes be uncoupled from verbal reporting.
Brain damage and functional localization
Strokes provide insight into brain–behavior relationships; deficits depend on damaged area.
The forebrain and beyond: major structures include the forebrain, midbrain, hindbrain.
Forebrain structures
Forebrain contains cerebral cortex and subcortical structures: thalamus, hypothalamus, pituitary, limbic system (emotion and memory circuit).
Cerebral cortex lobes: frontal, parietal, temporal, occipital.
Frontal lobe and language areas
Frontal lobe: reasoning, motor control, emotion, language; contains:
Motor cortex: movement planning and execution.
Prefrontal cortex: higher-level cognitive functioning.
Broca’s area: language production.
Classic cases:
Broca’s area damage → difficulty producing language.
Phineas Gage: frontal lobe damage leading to personality changes and impaired impulse control; highlighted the role of the frontal lobe in executive function.
Parietal lobe and somatosensory cortex
Somatosensory cortex processes touch, temperature, pain; topographic (somatotopic) organization mirrors the body map (Figure 3.20).
Temporal lobe
Involved in hearing, memory, emotion, language aspects.
Auditory cortex resides here; Wernicke’s area important for language comprehension.
Distinction: Broca’s area (production) vs. Wernicke’s area (comprehension).
Occipital lobe
Primary visual cortex; retinotopic organization maps visual field to cortex.
Other forebrain areas
Thalamus: sensory relay center (all senses except smell) routing to cortex.
Limbic system: emotion and memory; key structures include:
Hippocampus: learning and memory consolidation (explicit memory).
Amygdala: emotion processing and linking emotion to memory.
Hypothalamus: regulates homeostatic processes (temperature, appetite, blood pressure); interfaces with endocrine system; regulates sexual motivation/behavior.
Case studies and notable cases
Henry Molaison (H.M.): removal of hippocampus and amygdala reduced seizures but caused profound anterograde amnesia; memory formation for explicit memory impaired, but some procedural learning remained intact, illustrating hippocampus role in explicit memory consolidation.
Clive Wearing: demonstrates memory impairment linked to hippocampus damage; still retains some musical ability, illustrating dissociation between memory systems.
Midbrain and hindbrain structures (Figure 3.24, 3.25)
Midbrain: reticular formation (sleep/wake cycle, arousal, motor activity); substantia nigra and VTA (dopamine production; movement, mood, reward, addiction).
Hindbrain: brainstem components—medulla (autonomic functions like breathing, BP, heart rate), pons (connects brain to rest of nervous system; regulates sleep), cerebellum (balance, coordination, motor skills; procedural memory).
Neuroimaging and brain imaging techniques
CT (computed tomography): X-ray-based structural imaging to detect tumors, atrophy.
PET (positron emission tomography): metabolic activity; uses tracers to show active brain regions; limited temporal resolution; exposes to radiation; often combined with CT (CT/PET).
MRI: magnetic fields to image tissue structure; high spatial resolution.
fMRI: functional MRI; tracks blood flow/oxygenation to infer neural activity over time; superior temporal and structural detail relative to PET.
EEG (electroencephalography): measures electrical activity via scalp electrodes; high temporal resolution (milliseconds) but lower spatial resolution.
Summary of forebrain, midbrain, hindbrain organization (Figure 3.17)
Forebrain: cortex + subcortical structures (thalamus, limbic system).
Midbrain: reticular formation; substantia nigra; VTA.
Hindbrain: brainstem (medulla, pons); cerebellum.
3.5 The Endocrine System
What is the endocrine system?
Glands produce hormones, which are chemical messengers binding to receptors on target cells.
Unlike neurotransmitters, hormones travel through the bloodstream and have widespread effects.
Hormonal effects are generally slower to arise but longer lasting than neural signaling.
Major glands and their hormones (Figure 3.30; Table 3.2)
Hypothalamus: releases hormones that regulate pituitary; connects nervous and endocrine systems. Releasing and inhibiting hormones (e.g., oxytocin; TSH-related hormones).
Pituitary gland (the “master gland”): secretes messenger hormones that regulate other glands; also secretes growth hormone and endorphins.
Thyroid: secretes thyroxine (T4) and triiodothyronine (T3); regulates growth, metabolism, and appetite. Hyperthyroidism (e.g., Graves): high thyroxine, agitation, weight loss; hypothyroidism: fatigue, cold sensitivity.
Pineal gland: secretes melatonin; regulates biological rhythms.
Adrenal glands: secrete epinephrine and norepinephrine; involved in stress response and metabolism.
Pancreas: secretes insulin and glucagon; regulate blood glucose; insulin lowers glucose; glucagon raises glucose; diabetes involves insufficient insulin.
Gonads: ovaries (estrogen, progesterone) and testes (androgens, e.g., testosterone); mediate sexual motivation and behavior.
Function and regulatory principles
The hypothalamus–pituitary axis coordinates endocrine signaling.
Endocrine hormones regulate homeostasis, growth, metabolism, stress responses, reproduction, and sexual behavior.
Negative feedback and practical examples
Hormone secretion often regulated by negative feedback: once a hormone is released, it reduces subsequent release signals from hypothalamus/pituitary (keeps levels within a target range).
Example: oral contraceptives use low-dose estrogen/progestin to suppress ovulation via negative feedback on hypothalamus/pituitary.
Dig Deep: Athletes and anabolic steroids
Anabolic steroids mimic testosterone; used to enhance muscle mass, strength, and endurance in some athletes.
Risks include acne, heart problems, mood changes, aggression; banning by sports organizations due to health risks and unfair advantage.
Case reference: Alex Rodriguez (A-Rod) doping controversy illustrates sociocultural and financial implications.
Key terms (summary for 3.5)
master gland, hypothalamus, pituitary, endocrine glands, hormones, negative feedback, homeostasis, anabolic steroids, adrenal, pancreas, thyroid, gonads.
Cross-cutting concepts and connections
Gene–environment interplay across sections
Gene–environment interactions shape physical and psychological outcomes; the same genotype can yield different phenotypes depending on context (epigenetics).
Range of reaction and genetic–environmental correlations explain how environment shapes gene expression and behavior.
Epigenetics shows that environmental factors can modify gene expression without changes to DNA sequence.
Brain–behavior relationships
Localized brain damage (stroke, injury) and imaging studies reveal roles of specific brain regions (Broca’s/Wernicke’s areas, hippocampus, amygdala, thalamus, hypothalamus).
Behavioral consequences (language production, memory consolidation, emotion processing) illustrate functional specialization and integration across brain networks.
Ethical and societal implications
Race as a genetic category is complex; emphasis on ancestry and genetic diversity rather than race for research accuracy and social implications.
Use of brain imaging, genetics, and endocrinology in mental health raises considerations about privacy, stigma, and medical ethics.
Quick study prompts (from the chapter context)
What are the differences between genotype and phenotype? Provide examples.
Explain the sickle-cell example in terms of natural selection and regional malaria prevalence.
Distinguish between dominant and recessive alleles with Punnett square examples; explain homozygous vs heterozygous.
Define polygenic traits and provide two examples.
Describe the resting potential and the sequence of events during an action potential, including the role of the Nodes of Ranvier and saltatory conduction.
Compare and contrast agonists, antagonists, and reuptake inhibitors using neurotransmitters as examples.
List the major divisions of the CNS and PNS and summarize the functions of the sympathetic vs. parasympathetic branches.
Identify the four lobes of the cerebral cortex and the primary functions associated with each; name Broca’s and Wernicke’s areas.
Describe the limbic system’s key components (hippocampus, amygdala, hypothalamus) and their roles.
Explain the hypothalamus–pituitary axis and why the pituitary is called the master gland.
Discuss the differences between CT, PET, MRI, fMRI, and EEG in brain imaging, including what each best reveals and its limitations.
Vm^{rest} = -70\,\mathrm{mV},\quad Vm^{th} = -55\,\mathrm{mV},\quad V_m^{peak} = +30\,\mathrm{mV}
46 = 23 + 23