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19 Cards in this Set
- Front
- Back
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In order for true regeneration to occur, all of these must occur:
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a. Formation of an axonal growth cone b. Axon (or process) elongation or growth c. Reformation of appropriate synapses (or specialization) after reaching the target structure d. Restoration of function
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The cell body response to injury of the axon in PNS
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a. CHROMATOLYSIS
b. There is a "general" INCREASE IN PROTEIN SYNTHESIS c. growth-associated proteins (GAPs) |
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Cell body response to injury of the axon in CNS
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a. For most neurons in the brain and spinal cord, a. and b. given above (for the PNS) also occur b. There is, however, no sustained increase in the synthesis and transport of GAPs
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Changes in the proximal segment of the axon (the part still connected to the cell body) following injury in PNS
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a. proximal segment dies back from the point of injury
b. Then a "growth cone" forms (or "sprouts") c. Elongation of the axonal growth cone then proceeds; growth rate is approximately 1-2 mm/day |
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Changes in the proximal segment of the axon (the part still connected to the cell body) following injury in CNS
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a. Following axonal injury, the proximal segment dies back in a way similar to what is seen in the PNS b. A structure referred to as an “injury bulb” forms at the tip of the proximal end; it does not elongate, or it elongates over only a very short distance; the injury bulb appears to be a swelling and resealing of the membrane at the cut end of the axon c. No significant elongation or growth of the injured axon occurs d. If the neuron cell body of origin does not have axon collaterals which are capable of "sustaining" it, the neuron itself will die
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Changes in the injury site in axon of PNS
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a. At the area of injury, there is a compromise of the blood/nerve barrier
1) Monocytes, macrophages, etc. enter from the blood and phagocytose debris from the degenerating axon; removal of debris is relatively fast 2) Schwann cells proliferate and form scars |
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Changes in the injury site in axon of CNS
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a. At the injury site, the blood/brain barrier is compromised
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Changes in the distal segment of the injured axon in PNS
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a. Phagocytosis of debris
b. Schwann cells proliferate to form elongated tubes called Bands of Von Bungner c. Synapses may be reformed d. Under the best of conditions, some function may be restored |
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Changes in the distal segment of injured axon in CNS
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a. Removal of myelin breakdown products and axonal debris is much slower in the CNS than in the PNS (over a year after transection, debris may still be present) b. There is no formation of anything comparable to the Bands of Von Bungner in CNS distal segments c. The axon does not elongate; no regeneration occurs
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When do portions of spinal and cranial nerves (axons or processes) have the potential to regenerate
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if they are injured in their peripheral distribution and the regrowth or regeneration must occur only in the peripheral distribution. It does not matter where the cell bodies of origin are;
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Result of transaction of olfactory nerve
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Olfactory neurons do not regenerate their axons following injury, however; if the olfactory nerve is transected, there will be retrograde degeneration of the axon and the cell body, followed by replacement of the receptor cells (as the result of mitosis); the axons of the newly born cells will then grow into the olfactory bulb
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CNS neurons which can regenerate their axons
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neurons in the brainstem reticular formation which utilize monoamines as neurotransmitters (NE, DA, 5HT)
The nucleus locus coeruleus (NE) and raphe nuclei (5HT) in the brainstem are examples |
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is there better regeneration if the axons or nerves are crushed or cut? why?
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crushed leaves the epineural or dural sheath intact; if axons or the nerve are cut, ends need to be sutured together; there is far less regeneration if the ends are not close, even in non-mammalian vertebrates; can use tubing, etc. to bridge the gap
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why return to function after Stroke?:
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1 may be collateral circulation 2 “ischemic penumbra”, which is an area of compromised, but viable, tissue affected by the stroke and at risk for infarct from further ischemia,
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why return to funciton after injury of CNS
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1.relief of edema
2. 1. Unmasking: when some inputs to an area are lost, the postsynaptic cells may undergo an adjustment in their excitability; also formerly “silent” synapses or connections may then be expressed 2. Collateral “sprouting”: |
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Cell body changes after injury in PNS, CNS?
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Chromatolysis (Y, Y), increased protein synthesis (YY), sustained GAPS (YN)
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Proximal response after injury in PNS, CNS?
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Die back (YY), Growth cone (YN), axon growth (YN)
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changes at injury site in PNS, CNS?
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Compromise of blood/nerve/brain barrier (YY) Scar formation (YY)
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Distal segment changes after injury in PNS, CNS?
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Phagocytosis (fast, slow), Bands of von BungnerYN), Synapse reformation (YN), Some return of function (YN)
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