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PSYB65H3 (479)
Ted Petit (185)
Chapter 16

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Ted Petit

Chapter 16  Autopsy o When someone dies, it is performed on them o The purpose is to gain understanding and provide information on why the person died o Gives important information to researchers and physicians about how different diseases affect the body and can also be used to come up with treatments.  DEGENRATION o NECROSIS  Occurs when there is a failure to maintain homeostasis  Swelling and membrane bursting occur  The membranes of the organelles and vesicles also burst along with the membrane encasing the neuron.  This bursting is called lysis and it spills all the contents of the neuron into the extracellular fluid death of the neuron  Mostly it is called by sudden injuries, disruption to the ion channel and from infections  Can also occur following damage that accumulates slowly like from neurodegenerative diseases.  CAUSES:  ISCHEMIA o Disruption in blood flow  resulting from a stroke or CVA o Associated with disruptions in the energy pathways of neuron, which in turn can affect the ion channels. o Reduce or terminate ATP production in neurons  This in turn will result in the stoppage of sodium potassium pump  And thus the inability to regulate sodium-potassium levels following an action potential  Stop ATP production stop Na+ K+ pump inability to regulate Na+ and K+ levels o Disruption in regulating calcium and water  Results in accumulation of intracellular water  Results in swelling and potentially bursting of the membrane.  Ca+ and H2O excess intracellular water burst  Failure to regulate calcium problems in releasing neurotransmitters.  INJURY o Can be caused by TBI, stroke and also neurodegenerative diseases o Results in alterations in the release of glutamate o Glutamate is an excitatory amino acid neurotransmitter that is involved in almost every fast excitatory event in the NS o However, glutamate itself is quite toxic excitotoxicity both excite neurons and kill them o Primary neural death appears to occur right after the traumatic event when glutamate is released in excess this leads to a flow of events causing the release of more glutamate more death. o Calcium can play a role as well  Secondary Neural death following the primary neural death; results from a large-scale influx of Ca+ into the neuron  Because glutamate can control ion channels as well, high release of glutamate results in excessive influx on Ca+ o APOPTOSIS  Is programmed neural death, in which the neuron uses its own machinery to ensure its own death.  Characterized by dead cells, in which the nucleus is condensed into a tangle of DNA  Can be initiated by  Damage to the DNA  Damage caused by free radicals  Withdrawal of tropic factors required for normal development  Presence of necrotic neurons  The process:  Typically triggered by genes  Which triggers the proteins known as caspases that are responsible for the death of the neuron  REGENERATION o In the CNS, neurogenesis does not occur, thus 2 processes act as compensatory mechanism  COLLATERAL SPROUTING  Undamaged neurons sprout new axon collaterals (side branches of axons) to innervate targets.  Collateral sprouting shows the brain’s ability to demonstrate its plasticity (to change in response to events in the environment)  Example: when one receive less info through the left eye, the ocular dominance columns of the right eye gets larger  This plasticity has a critical period; usually not seen in adults  REGENRATIVE SPROUTING  Regeneration only occurs within the peripheral nervous system  Axotomy: cutting off an axon the PNS recovers but the CNS does not  Events like spinal cord injuries that lead to Axotomy results in the permanent loss of the neuron and the function  WHY? o One hypothesis is that CNS is just not capable of regeneration o The environment of the CNS does not permit regeneration  PNS and CNS axons differs in terms of the glia that surrounds them  PNS axons are myelinated by Schwann cells and CNS axons are myelinated by oligodendrocytes  If a piece of the PNS nerve tissue or Schwann cells is transplanted into the CNS at the site of injury, it will regenerate until it touches the CNS tissue. o The location seems to be a factor as well  When it is closest to the PNS and axons that interface with the PNS, axon regeneration seems to the strongest. o Conclusion Glia (astrocytes and oligodendrocytes) inhibit axon regeneration in CNS  NEUROGENESIS  Much of the neurogenesis occurs before birth and even if it happens after birth, its usually immediately after birth  However, there ar
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