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首页> 外文期刊>journal of neuropathology and experimental neurology >CYTOLOGIC OBSERVATIONS ON AXOTOMIZED FELINE BETZ CELLS1period; QUALITATIVE ELECTRON MICROSCOPIC FINDINGS
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CYTOLOGIC OBSERVATIONS ON AXOTOMIZED FELINE BETZ CELLS1period; QUALITATIVE ELECTRON MICROSCOPIC FINDINGS

机译:CYTOLOGIC OBSERVATIONS ON AXOTOMIZED FELINE BETZ CELLS1period; QUALITATIVE ELECTRON MICROSCOPIC FINDINGS

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摘要

Adult cats survived left lateral funiculotomy 1 to 153 days. The pericruciate cortex was studied electron microscopically in these as well as sham-operated and unoperated animals. Ten days after surgery Betz cells of the right pericruciate cortex displayed disaggregation of cytoplasmic ribosomes; random dispersal and degranulation of the normally compact arrays of cisterns of rough ER; in some cells perinuclear and peripheral disposition of remaining Nissl bodies; retispersion of the Golgi apparatus; and, uncommonly, neurofilamentous hyperplasia. Fourteen days postoperatively cytoplasmic ribosomes were largely regrouped in rosette arrangements and Golgi membranes were evenly distributed in the cytoplasm. Further reversion of the ER toward a normal appearance occurred 28 days postoperatively but substantial perikaryal atrophy had supervened in many neurons by 49ndash;153 days after surgery. Evidence of nerve cell death was not found. Concentric membranous arrays derived from ER and associated with autophagic bodies and mitochondria were identified in dendrites of normals and cats that had been operated upon, perhaps more frequently contralateral to the spinal operation. Electron-dense and electronlucent degenerative changes in dendrites also occurred, especially early after operation. Degenerating myelin sheaths were detected in the pericruciate cortex of animals that had been operated upon and sometimes were captured in the process of phagocytosis by oligodendrocytes as well as astrocytes and microglia. The long-term persistence of axotomized Betz cells, albeit in an atrophic state, and the reversibility of some of the cytologic responses to axon injury suggest that these neurons may retain a capacity for axon regeneration that could be mobilized, as by pharmacologic means.

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