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Rate of climbing fiber degeneration in rabbit cerebellum following parafloccular stalk and medullopontine lesions
Author(s) -
Mejia Hugo
Publication year - 1976
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.901650404
Subject(s) - cerebellum , anatomy , biology , climbing , cerebellar cortex , white matter , degeneration (medical) , climbing fiber , lesion , cortex (anatomy) , pathology , neuroscience , medicine , magnetic resonance imaging , ecology , radiology
To resolve inconsistencies in experimental studies which use reduced silver methods to detect cerebellar climbing fiber sources within the brain stem, an evaluation of the temporal course of degeneration was undertaken. The paraflocculus of the rabbit is uniquely situated within the temporal bone and connects with the corpus cerebelli via a stalk passing through a bony foramen. A unilateral electrolytic lesion deafferented the paraflocculus without disturbing blood supply or causing other damage (18 animals). Comparatively, another group of unilateral lesions was placed at the dorsolateral pontomedullary junction, adding significantly to the cortical area deafferented (12 animals). Animals of each group were killed at successively longer intervals commencing at 18 hours, and a modified Fink‐Heimer impregnation process was applied to the cerebellar cortex and opposite‐sided controls. In parafloccular lesions, degeneration was detected at 24 hours in the climbing fibers of the molecular layer. At successively longer intervals, degeneration became increasingly evident in granule layer and white matter. Subsequent to dorsolateral pontomedullary lesions, climbing fiber degeneration was first observed in the molecular layer at 24 hours and was clearly evident there at 36 hours. By 72 hours degeneration had reached the white matter, meanwhile disappearing in the molecular layer where it was first seen. Using techniques of Nauta‐Fink‐Heimer to display secondary climbing fiber degeneration in cerebellar cortex, it was found that too long post‐operative intervals could preclude its detection, since in both groups of animals it commenced earlier and disappeared sooner in the molecular layer.

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