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Long-term status of pyramidal cell axon collaterals and apical dendritic spines in denervated cortex.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Rutledge, Lester T. Duncan, John A. T. Cant, Nell B. |
| Copyright Year | 1972 |
| Abstract | Some central nervous system neurons when deafferented and deefferented (denervated) undergo progressive degeneration leading to cellular death and resorption of neuronal debris. In others, in what appears to be compensatory new growth, axonal proliferation is seen1,12. Whether proliferation occurs depends upon such critical factors as neuronal age, type and location of neurons and probably whether deafferentation has been complete or partial. The latter must be especially important since presynaptic impingement upon a partially deafferented neuron likely determines whether cytoplasmic metabolic pathways remain functional. A most fundamental problem relative to proliferation of axonal processes is whether the neoformations effect structural and functional contact with neighboring neurons. If such contacts are not established then the new growth is of little interest in the consideration of reorganization within the nervous system following injury. It is possible where proliferation has been observed, that rather than additional new growth, neurons were expressing a maintenance of protoplasmic mass, a feature inherent in the constitution of certain neuronal tissues 1. In the cerebral cortex of neonatal cats (likely also at least in dogs), if a cut is made slightly below gray matter (cortex undercut), axon collateral proliferation of pyramidal cells may be observed within a few days1,12. One or more collaterals from the truncated axon grow recurrently in a branching manner among neighboring cellular processes giving the appearance of arciform or short axon neurons 12. However, the changes may involve only thickening or hypertrophy of collateral trunks1,18. Nearly 70 years ago Cajal astutely observed that axonal proliferation toward nearby neurons might preserve the nervous impulse in the injured neuron and actually 'in- |
| Starting Page | 695 |
| Ending Page | 704 |
| Page Count | 10 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | https://deepblue.lib.umich.edu/bitstream/handle/2027.42/34082/0000361.pdf?isAllowed=y&sequence=1 |
| Alternate Webpage(s) | https://deepblue.lib.umich.edu/bitstream/handle/2027.42/34082/0000361.pdf?sequence=1 |
| PubMed reference number | 5038328v1 |
| Volume Number | 41 |
| Issue Number | 2 |
| Journal | Brain research |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | Assumed Axon collateral Body tissue Brain CNS disorder Canis familiaris Cerebral cortex Deafferentation procedure Dendritic Spines Denervation Description Gray Matter Hypertrophy Infiltration Nervous system structure Neuroglia Neurons Pyramidal Cells Resorption Seizures Telling untruths Tissue fiber Vertebral column negative regulation of MAPK cascade involved in axon regeneration |
| Content Type | Text |
| Resource Type | Article |
