Mind, Brain & BehaviorFriday

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 SystemChapter 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. Ca2 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.