Reorganization in granuloprival cerebellar cultures after transplantation of granule cells and glia. I. Light microscopic and electrophysiological studies

1983 ◽  
Vol 214 (3) ◽  
pp. 258-266 ◽  
Author(s):  
Fredrick J. Seil ◽  
Arnold L. Leiman ◽  
Nathan K. Blank
2001 ◽  
Vol 85 (5) ◽  
pp. 1847-1857 ◽  
Author(s):  
J. R. Mellor ◽  
A. D. Randall

GABA concentration jump experiments performed on membrane patches predict that postsynaptic GABAAreceptors will become desensitized following the release of the contents of a single GABA-containing synaptic vesicle. To examine this we used a single synaptic bouton stimulation technique to directly examine whether postsynaptic GABAA receptors in cultured cerebellar granule cells exhibit transmitter-induced desensitization. In a large number of recordings, no evidence was found for desensitization of postsynaptic GABAAreceptors by vesicularly released transmitter. This was the case even when as many as 40 vesicles were released from a single bouton within 1.5 s. In addition, postsynaptic depolarization and application of the benzodiazepine flunitrazepam, manipulations previously shown to enhance desensitization of GABAA receptors, failed to unmask transmitter-induced desensitization. In contrast, a single 2- to 3-s application of a high concentration of exogenous GABA was able to depress synaptic responsiveness for up to 70 s. Furthermore, pharmacological depletion of GABA eliminated inhibitory synaptic communication, suggesting that GABA is the transmitter and the desensitization-resistant inhibitory postsynaptic currents are not mediated by a “nondesensitizing” ligand such as β-alanine. Overall our data indicate that a specific desensitization-resistant population of GABAA receptors are present at postsynaptic sites on cultured cerebellar granule cells.


1998 ◽  
Vol 45 (3) ◽  
pp. 781-790 ◽  
Author(s):  
E M Sajdel-Sulkowska

Expression of CD15 antigen (also referred to as stage specific embryonic antigen, SSEA-1, or Lewis(x)) was analyzed in cerebellar cultures prepared from seven day old rats by double immunostaining with anti-CD15 mAb7A and cell-specific antibodies to glial fibrillary acidic protein (GFAP) and Vimentin. The immunocytochemical data suggest that the expression of CD15 antigen is restricted to some GFAP-positive cells with fibroblast-like morphology characteristic of Type-1 astrocytes. In order to explore the involvement of CD15 antigen in glial-neuronal interactions, the ability of mAb7A antibody to interfere with granule cell adhesion to a monolayer of astrocytes was tested in comparison with anti-GFAP. The adhesion of cerebellar granule cells to astrocytes, as determined by the number of bound cells, was decreased by 39% following preincubation with mAb7A. Anti-GFAP did not alter cell adhesion, indicating the specificity of the anti-CD15 antibody effect. These results are consistent with the hypothesis that CD15 antigen participates in glial-neuronal interactions in the developing cerebellum. Furthermore, it may be speculated that the modulation of cell-surface CD15 expression contributes to the altered strength of glial-neuronal interaction, facilitating cell migration and differentiation.


1970 ◽  
Vol 45 (2) ◽  
pp. 212-220 ◽  
Author(s):  
Fredrick J. Seil ◽  
Robert M. Herndon

The behavior of granule cells in mature cerebellar cultures derived from newborn mice was studied by light and electron microscopy. Many granule cells remained in the explants as an external granular layer. These cells were differentiated, as evidenced by formation of bundles of parallel fibers and by development of synapses between granule cell axons and Purkinje cell branchlet spines, and between Golgi cell axons and granule cell dendrites. Although the over-all architecture of the cerebellar explants after 18–33 days in vitro was similar to that of the newborn mouse, the evident differentiation of the granule cells suggested that interneuronal relationships resemble those of the mature cerebellum in vivo.


Author(s):  
R.V.W. Dimlich ◽  
M.H. Biros

Although a previous study in this laboratory determined that Purkinje cells of the rat cerebellum did not appear to be damaged following 30 min of forebrain ischemia followed by 30 min of reperfusion, it was suggested that an increase in rough endoplasmic reticulum (RER) and/or polysomes had occurred in these cells. The primary objective of the present study was to morphometrically determine whether or not this increase had occurred. In addition, since there is substantial evidence that glial cells may be affected by ischemia earlier than other cell types, glial cells also were examined. To ascertain possible effects on other cerebellar components, granule cells and neuropil near Purkinje cells as well as neuropil in the molecular layer also were evaluated in this investigation.


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