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Chapter 16

PSYB65 - Chapter 16 - Nov 15, 2010

4 Pages
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Department
Psychology
Course Code
PSYB65H3
Professor
Ted Petit

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Chapter 16: Recovery of Function
Module 16.1: Neural Degeneration, Regeneration, Reorganization
DEGENERATION
-All cells, including neurons, die in one of two ways:
1. Necrosis – when there is an overwhelming failure to maintain homeostasis within the neuron
2. Apoptosis – programmed neural death, in which the neuron uses its own machinery to ensure
its own death
Necrosis (Abnormal event)
-When neurons completely lose their ability to regulate their internal environment (homeostasis),
swelling and membrane bursting occur. This bursting / lysis spills the contents of the neuron into
the extracellular space, which results in the death of the neuron.
-Often associated with damage that occurs rapidly, e.g. mechanical damage to the neurons, events
that cause disruption to ion channels, or the results of inflection. It can also follow damage that
accumulates more slowly.
-Common causes:
1. Ischemia (disruption in blood flow that often results from a stroke/cerebrovascular accident)
Affect ion channels that are important for homeostasis in the neuron (e.g. reduce/terminate
ATP production in the neuron)
Failure to maintain homeostatic levels of sodium and potassium will disrupt the neurons
ability to regulate calcium and water, and will have disastrous effects for the neuron.
Failure to regulate water accumulation of intracellular water neurons swelling and
potentially breaking its membrane cover
Failure to regulate intracellular calcium concentrations problems for the release of
neurotransmitters
2. Acquired injury
Both TBI and strokes, and neurodegenerative disease have elements of necrotic cell death
Excitotoxcity – ability of specific compounds, e.g. glutamate, to both excite neurons and kill
them. Glutamate is an excitatory amino acid neurotransmitter that is involved in almost every
fast excitatory event in the nervous system, which is toxic to neurons and glia.
Primary neural death – death of neurons that occurs immediately after trauma, appears to
occur when glutamate is released in excess. (can result from the neurons exhausting its
resources and overwhelming homeostatic mechanisms)
Secondary neuronal death – death of neurons following the primary event; results from a
large-scale influx of calcium into the neuron glutamate can regulate a calcium channel 
excess release of glutamate sustained and excessive influx of calcium
-Major events lead to necrosis: (1) changes in intracellular concentrations of ions, e.g. calcium (2)
changes in the ability of the neuron to produce energy, e.g. ATP (3) damage to the organelles of the
neuron, e.g. mitochondria
Apoptosis (Normal development of neuron)
-Active process that uses cellular energy to effect death
-Characterized by dead cells in which the nucleus is condensed into a tangle of DNA fragments, and
also intact cell membranes.
-Can be initiated in a variety of ways, including damage to the DNA of the neuron, damage caused
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Description
Chapter 16: Recovery of Function Module 16.1: Neural Degeneration, Regeneration, Reorganization DEGENERATION - All cells, including neurons, die in one of two ways: 1. Necrosis when there is an overwhelming failure to maintain homeostasis within the neuron 2. Apoptosis programmed neural death, in which the neuron uses its own machinery to ensure its own death Necrosis (Abnormal event) - When neurons completely lose their ability to regulate their internal environment (homeostasis), swelling and membrane bursting occur. This bursting lysis spills the contents of the neuron into the extracellular space, which results in the death of the neuron. - Often associated with damage that occurs rapidly, e.g. mechanical damage to the neurons, events that cause disruption to ion channels, or the results of inflection. It can also follow damage that accumulates more slowly. - Common causes: 1. Ischemia (disruption in blood flow that often results from a strokecerebrovascular accident) Affect ion channels that are important for homeostasis in the neuron (e.g. reduceterminate ATP production in the neuron) Failure to maintain homeostatic levels of sodium and potassium will disrupt the neurons ability to regulate calcium and water, and will have disastrous effects for the neuron. Failure to regulate water accumulation of intracellular water neurons swelling and potentially breaking its membrane cover Failure to regulate intracellular calcium concentrations problems for the release of neurotransmitters 2. Acquired injury Both TBI and strokes, and neurodegenerative disease have elements of necrotic cell death Excitotoxcity ability of specific compounds, e.g. glutamate, to both excite neurons and kill them. Glutamate is an excitatory amino acid neurotransmitter that is involved in almost every fast excitatory event in the nervous system, which is toxic to neurons and glia. Primary neural death death of neurons that occurs immediately after trauma, appears to occur when glutamate is released in excess. (can result from the neurons exhausting its resources and overwhelming homeostatic mechanisms) Secondary neuronal death death of neurons following the primary event; results from a large-scale influx of calcium into the neuron glutamate can regulate a calcium channel excess release of glutamate sustained and excessive influx of calcium - Major events lead to necrosis: (1) changes in intracellular concentrations of ions, e.g. calcium (2) changes in the ability of the neuron to produce energy, e.g. ATP (3) damage to the organelles of the neuron, e.g. mitochondria Apoptosis (Normal development of neuron) - Active process that uses cellular energy to effect death - Characterized by dead cells in which the nucleus is condensed into a tangle of DNA fragments, and also intact cell membranes. - Can be initiated in a variety of ways, including damage to the DNA of the neuron, damage caused www.notesolution.com
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