Mind, Brain & Behavior Friday January 24, 2003

Cerebral Cortex  Outer layers of cortex – gray matter  Underlying myelinated axons and glial cells – white matter  Clusters of related neurons – called nuclei: Basal ganglia Hippocampus Amygdala  Two hemispheres

Four Functional Lobes  Frontal  Parietal  Temporal  Occipital  Two other areas: Insular cortex – inside the lateral sulcus Limbic lobe – inside the four lobes overlying the brain stem and diencephalon

Deep-Lying Structures  Basal Ganglia – regulation of movement, cognition. Receive input from all four lobes and communicate to the frontal cortex via thalamus.  Hippocampus – forms memories  Amygdala – coordinates emotion, autonomic and endocrine systems via hypothalamus. Hippocampus & amygdala are parts of limbic system.

Four Organizational Principles  Each system contains relay centers (nuclei). Relay nuclei contain local interneurons and projection interneurons. Thalamus – processes almost all sensory info  Each system has several distinct pathways.  Pathways are topographically organized.  Most pathways cross to the opposite side. Decussation

Systems Interact  Textbook example: physical actions involve sensory, motor and limbic (motivational) systems. When systems interact, they must be interconnected (see Figure 5-9) Different senses have their own pathways operating in parallel. Information is combined (integrated) at some point -- how this happens is an open question.

Development of the Nervous System Chapter 6

Neural Development  Three developmental stages: Cell proliferation Cell migration Cell differentiation  Developed cell must: Send axons down the right pathways Terminate at the right target Choose the correct cells to synapse with within that target

How Cells Develop  Stem cells divide to form new neurons. All of the brain’s neocortical neurons are formed before birth.  The type of cell (glia vs. various kinds of neurons) depends on the environment when it is “born.”  Immature neurons are called neuroblasts.

Migration and Differentiation  Neuroblasts migrate up radial glia to the cortical plate where they begin to form neurites (axons and dendrites).  Neurons in the cortical plate then become the layers of the cortex, beginning with layer VI (lowest layer).  Neuroblasts will differentiate even if removed from the cortex.  Many more neurons are created than will survive cell die off.

Connections Among Neurons  The growing tip of an axon is called a growth cone.  Lamellipodia – flaps at the edge of the growth cone. Fold in to become the terminal synapse at destination. Filopodia – spikes take hold of the extracellular material and pull the cone forward.

Pathway Formation  Axons stick together due to fasciculation – expression of cell adhesion molecules (CAM).  Chemical markers in the axon and the targets guide axon growth.  Diffusable molecules called netrins also attract axons.  Absence of laminin at target may retard further growth.

Synapse Formation  Proteins are secreted by both the growth cone and the target membrane in a layer – basal lamina.  Interaction between these proteins results in receptor formation. Agrin reception attracts ACh receptors. Ca 2 enters the growth cone and triggers neurotransmitter release.

Naturally Occurring Cell Die Off  Cells compete to innervate targets. Those not used die off.  Cell survival depends on activation at the target.  Neurotrophins travel back from target tissue to neuron cell body promoting survival. Nerve growth factor (NGF) Brain-derived neurotrophic factor (BDNF).

Activity-Dependent Rearrangement  At first cells are in no particular order and send axons everywhere.  Neural activity causes rearrangement of cells and synapses.  Hebb synapses – synapses that are active at the same time as the target is active are strengthened. Things that fire together, wire together.

Plasticity  Critical periods are periods of plasticity.  Plasticity ends when axon growth ends.  Plasticity ends when synaptic transmission matures.  Plasticity diminishes when cortical activation is constrained. Reduction of ACh or NE (norepinephrine)

Aging and the Brain  To study normal aging of the brain, researchers must control for health conditions.  Abnormal aging is affected by: Dementia – usually caused by artherosclerosis (hardening of arteries) Alzheimer’s disease

Causes of Brain Cell Loss  Shrinkage averages 10% over lifespan, due to decreased neuron density (shrunken neurons).  Causes of cell loss are not age but: Medication, chronic disease (esp. heart disease) Alcohol, high blood pressure in middle age Grief, absence of stimulating partner Sedentary lifestyle, inflexible personality, lack of stimulation, lack of learning & curiosity Malnutrition, depression

Mental Changes in Old Age  Cognitive processes slow down Neuronal speed of transmission may be affected by loss of myelin NMDA receptors decrease by 30% (important to learning & memory)  Variability across different individuals is greater at 60 than at other times of life.  Loss of functioning is relative to someone’s original level of functioning.

Longitudinal Studies  Scores on IQ tests show little decline until age 70.  Declines in motor movements are not dramatic or disabling.  Remaining intellectually active protects against some cognitive decline. Elderly professors do better than same-age controls, even on memory tasks.

Sensory Loss  Age-related changes in hearing and vision can affect performance.  Decline in sensory acuity affects: Amount of information received Rate at which information can be processed

Behavioral Consequences  Most elderly compensate for the gradual changes during aging so that no performance difference occurs.  Other ways can be found to do most tasks.  Elderly may continuously increase in “wisdom,” social and emotional skills, experience-based understanding.