Transcript Mind, Brain & Behavior

Mind, Brain & Behavior
Friday
January 24, 2003
Cerebral Cortex
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Outer layers of cortex – gray matter
Underlying myelinated axons and glial cells –
white matter
Clusters of related neurons – called nuclei:
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Basal ganglia
Hippocampus
Amygdala
Two hemispheres
Four Functional Lobes
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Frontal
Parietal
Temporal
Occipital
Two other areas:
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Insular cortex – inside the lateral sulcus
Limbic lobe – inside the four lobes overlying the
brain stem and diencephalon
Deep-Lying Structures
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Basal Ganglia – regulation of movement,
cognition.
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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.
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Hippocampus & amygdala are parts of limbic
system.
Four Organizational Principles
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Each system contains relay centers (nuclei).
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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.
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Decussation
Systems Interact
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Textbook example: physical actions involve
sensory, motor and limbic (motivational)
systems.
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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
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Three developmental stages:
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Cell proliferation
Cell migration
Cell differentiation
Developed cell must:
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Send axons down the right pathways
Terminate at the right target
Choose the correct cells to synapse with within that target
How Cells Develop
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Stem cells divide to form new neurons.
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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
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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
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The growing tip of an axon is called a growth
cone.
Lamellipodia – flaps at the edge of the growth
cone.
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Fold in to become the terminal synapse at
destination.
Filopodia – spikes take hold of the extracellular
material and pull the cone forward.
Pathway Formation
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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
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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.
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Agrin reception attracts ACh receptors.
Ca2 enters the growth cone and triggers
neurotransmitter release.
Naturally Occurring
Cell Die Off
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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.
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Nerve growth factor (NGF)
Brain-derived neurotrophic factor (BDNF).
Activity-Dependent Rearrangement
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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.
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Things that fire together, wire together.
Plasticity
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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.
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Reduction of ACh or NE (norepinephrine)
Aging and the Brain
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To study normal aging of the brain,
researchers must control for health conditions.
Abnormal aging is affected by:
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Dementia – usually caused by artherosclerosis
(hardening of arteries)
Alzheimer’s disease
Causes of Brain Cell Loss
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Shrinkage averages 10% over lifespan, due to
decreased neuron density (shrunken neurons).
Causes of cell loss are not age but:
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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
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Cognitive processes slow down
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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
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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.
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Elderly professors do better than same-age
controls, even on memory tasks.
Sensory Loss
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Age-related changes in hearing and vision can
affect performance.
Decline in sensory acuity affects:
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Amount of information received
Rate at which information can be processed
Behavioral Consequences
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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.