Genetics, Development, & Plasticity

Genetics and Behavior

• Genes and environment interact to shape behavior.
• The key question is the extent of each factor's influence.
• Examples include facial expressions, psychological disorders, weight gain, personality, and sexual orientation.

How DNA Controls Development

• Proteins determine body development.
  • Forming structural components.
  • Serving as enzymes (biological catalysts) regulating chemical reactions.

Sex-Linked and Sex-Limited Genes

• Autosomal genes: all genes except sex-linked.
• Sex-linked genes: genes on sex chromosomes (X and Y in mammals).
• Females: XX chromosomes.
• Males: XY chromosomes.

Mendelian Genetics—X and Y

• During reproduction:
  • Females contribute an X chromosome.
  • Males contribute X or Y, determining sex.
• Male X contribution → genetically female offspring.
• Male Y contribution → genetically male offspring.

Epigenetics

• Changes in gene expression without DNA sequence modification.
• Genes active at specific times (life stage, time of day, etc.).
• Crucial to learning and memory.
• Explains differences in monozygotic twins.

Heredity and Environment

• Almost all behaviors have both genetic and environmental components.
• Research methods:
  • Twin studies (monozygotic vs. dizygotic).
  • Adoption studies (resemblance to biological parents).
  • Identifying specific genes linked to behaviors.

Environmental Modification

• Traits with strong hereditary influence can be modified.
• Example: PKU (phenylketonuria), a genetic inability to metabolize phenylalanine.
• Environmental interventions can modify PKU effects.

How Genes Affect Behavior

• Genes don't directly produce behaviors.
• They produce proteins that increase the probability of a behavior under certain conditions.
• Indirect effects: genes alter the environment by influencing how others react to an individual.

Behavior and Natural Selection

• Some behaviors' relation to natural selection is debated.
• Examples:
  • Lifespan length.
  • Gender differences in sexual promiscuity.
  • Altruistic behavior (benefiting others at a cost to oneself; rare outside humans).

Maturation of the Vertebrate Brain

• The central nervous system forms around 2 weeks of embryonic development.
• The dorsal surface thickens, forming a neural tube with a fluid-filled cavity.
• The forward end differentiates into hindbrain, midbrain, and forebrain.
• The rest of the neural tube becomes the spinal cord.

Human Brain Development

• At birth: ~350 grams.
• By the first year: ~1000 grams.
• Adult brain: 1200–1400 grams.

The Development of Neurons

• Processes involved:
  • Proliferation
  • Migration
  • Differentiation
  • Myelination
  • Synaptogenesis

1. Proliferation

• Production of new cells/neurons early in life.
• Cells lining ventricles divide.
  • Some become stem cells (continue dividing).
  • Others become neurons or glia, migrating to other locations.

2. Migration

• Movement of new neurons and glia to final locations.
• Some reach destinations in adulthood.
• Occurs in various directions.
• Guided by immunoglobulins and chemokines.

3. Differentiation

• Formation of axon and dendrites, giving neurons distinctive shapes.
• Axon grows first (during migration or after reaching target), followed by dendrites.

4. Myelination

• Glia produce fatty sheath covering some axons.
• Speeds up neural impulse transmission.
• Occurs first in spinal cord, then hindbrain, midbrain, forebrain.
• Gradual process lasting decades.

5. Synaptogenesis

• Formation of synapses between neurons.
• Occurs throughout life; neurons constantly form and discard connections.
• Slows significantly later in life.

New Neurons Later in Life

• Initially believed no new neurons formed after early development.
• Later research showed otherwise.
• Stem cells: undifferentiated cells in the brain's interior that generate daughter cells (glia or neurons).
• New olfactory receptors continuously replace dying ones.
• Stem cells differentiate into new neurons in the adult hippocampus, facilitating learning.

The Life Span of Neurons

• Different cells have different average life spans.
• Skin cells: newest (most under a year old).
• Heart cells: tend to be as old as the person.
• Mammalian cerebral cortexes form few/no new neurons after birth.

Pathfinding by Axons

• Axons travel long distances to form correct connections.
• Sperry’s (1954) research (newts) showed axons follow chemical trails.
• Growing axons reach targets by following chemical gradients; attracted by some, repelled by others.

Specificity of Axon Connections

• Axons regrow and attach to the same target neurons as before, maintaining the original mapping.

Competition among Axons

• Initially, axons form synapses with multiple cells.
• Postsynaptic cells strengthen some connections, eliminate others.
• Formation/elimination depends on input from incoming axons.
• More connections are formed initially than needed.
• Successful axon connections survive; others fail to sustain active synapses.

Determinants of Neuronal Survival

• Levi-Montalcini: muscles determine how many axons survive, not form.
• Nerve growth factor (NGF): protein released by muscles promoting axon survival and growth.
• Brain overproduces neurons, then uses apoptosis to match incoming axons to receiving cells.
• Axons not exposed to neurotrophins undergo apoptosis (preprogrammed cell death).
• Healthy adult nervous system has no neurons that failed to connect.

Fetal Alcohol Syndrome

• Condition in children born to mothers who drank heavily during pregnancy.
• Marked by:
  • Hyperactivity and impulsiveness.
  • Difficulty maintaining attention.
  • Varying degrees of mental retardation.
  • Motor problems and heart defects.
  • Facial abnormalities.
• Dendrites are short with few branches.
• Alcohol suppresses glutamate, enhances GABA release.
• Neurons receive less excitation/neurotrophins, undergo apoptosis.

Differentiation of the Cortex

• Neurons in different brain areas differ in shape and chemical components.
• Immature neurons transplanted to a developing cortex area develop the properties of the new location.
• Later-stage transplants develop some new properties but retain some old ones.
• Example: ferret experiment.

Changes in Dendritic Trees

• Gain/loss of spines indicates new connections (related to learning).
• Measurable neuronal expansion in humans with physical activity.
• As old neurons die (apoptosis) and new ones form, learning and memory improve.

Experience and Dendritic Branching

• Old belief: teaching difficult concepts enhances intelligence in other areas ("far transfer").
• Evidence shows only skills associated with the practiced task transfer.
• The brain cannot be "exercised" like a muscle.

Effects of Special Experiences

• Blind people improve attention to touch and sound with practice.
• Touch information activates the occipital cortex (normally for vision).
• The occipital lobe adapts to process tactile and verbal information.
• People blind from birth are better at discriminating objects by touch; increased occipital cortex activation during touch tasks.

When Brain Reorganization Goes Too Far

• Focal hand dystonia/"musician's cramp": excessive brain reorganization.
• Musicians' fingers become clumsy, fatigue easily, make involuntary movements.
• Results from sensory thalamus and cortex reorganization, causing touch responses of one finger to overlap with others.

Brain Development and Behavioral Development

• Adolescents are more impulsive than adults.
• Impulsivity can lead to risky behaviors.
• Adolescents tend to "discount the future."
• Prefrontal cortex is relatively inactive in certain situations (may or may not cause impulsivity).
• Impulsivity varies depending on peers, decision time, etc.

Plasticity after Brain Damage

• Most survivors show some behavioral recovery.
• Recovery relies on new axon and dendrite branches.
• Causes of brain damage:
  • Tumors
  • Infections
  • Exposure to toxic substances or radiation
  • Degenerative diseases
  • Closed head injuries

Brain Damage and Immediate Treatments

• Closed head injury: sharp blow to the head without puncturing the brain; common in young adults.
• Recovery can be slow and incomplete after severe injury.
• Stroke/cerebrovascular accident: temporary loss of blood flow to the brain; common in the elderly.

Types of Strokes

• Ischemia: most common; from blood clot or artery obstruction; neurons lose oxygen and glucose.
• Hemorrhage: less frequent; from ruptured artery; neurons flooded with excess blood, calcium, oxygen, etc.

Effects of Strokes

• Ischemia and hemorrhage cause:
  • Edema: fluid accumulation in the brain, increasing pressure and stroke risk.
  • Disruption of sodium–potassium pump: potassium accumulates inside neurons.
• Edema and excess potassium trigger glutamate release.
• Excess positive ions block metabolism in mitochondria, killing the neuron.

Immediate Treatments for Stroke

• Tissue plasminogen activator (tPA): breaks up blood clots, reducing ischemic stroke effects.
• Research focuses on blocking glutamate synapses and calcium entry.
• Cooling the brain minimizes damage.
• Cannabinoids may minimize cell loss (most effective in lab animals when taken before the stroke).

Later Mechanisms of Recovery

• Surviving brain areas increase/reorganize activity.
• Diaschisis: decreased activity of surviving neurons after functional loss of other neurons.
• Damage disrupts normal stimulation patterns.
• Stimulants may activate healthy brain regions.
• Destroyed cell bodies cannot be replaced, but damaged axons can regrow.

Regrowth of Axons

• Damaged axons do not readily regenerate in mature mammalian brains/spinal cords.
• Scar tissue forms a mechanical barrier.
• Neurons pull apart at the site of the cut.
• Glia cells release chemicals inhibiting axon growth.
• Research on building protein bridges may help.

Axon Sprouting

• Collateral sprouts: new branches from non-damaged axons attaching to vacant receptors.
• Cells that lost innervation release neurotrophins, inducing sprout formation.
• Sprouts fill vacated synapses over months (can be useful, neutral, or harmful).

Reorganized Sensory Representations and the Phantom Limb

• Phantom limb: continued sensation of an amputated body part.
• The cortex reorganizes after amputation, responding to other body parts.
• Original axons degenerate, leaving vacant synapses for new sprouts.

Sources of Phantom Sensation

• Reorganization of the somatosensory cortex, leading to sensations from other body parts being misinterpreted as coming from the missing limb. The homunculus illustrates the mapping of body parts onto the somatosensory cortex.

Learned Adjustments in Behavior

• Deafferentated limb: limb that has lost afferent sensory input.
• Can still be used, but other mechanisms are easier.
• Therapy techniques developed to improve functioning in brain-damaged people.
• Focuses on what they are capable of doing.