Senescent changes in a neurobiological model system: Cerebellar Purkinje cell electrophysiology and correlative anatomy
Senescent changes in a neurobiological model system: Cerebellar Purkinje cell electrophysiology and correlative anatomy
复制标题
神经生物学模型系统的衰老变化:小脑浦肯野细胞电生理学和相关解剖学
DOI:
10.1016/0197-4580(80)90018-4
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发表时间:
1980
影响因子:
4.2
通讯作者:
F. Bloom
中科院分区:
文献类型:
--
作者:
J. Rogers;M. Silver;W. Shoemaker;F. Bloom
A within-subjects design was used to assess age changes in cerebellar Purkinje neurons. Four groups of naive male Sprague-Dawley rats, aged 3, 10, 20, and 28 months, underwent single cell recording for electrophysiological assessment of Purkinje cell firing patterns, followed by perfusion for glyoxylic acid induced catecholamine fluorescence. Cerebellar sections were photographed first by fluorescence microscope for catecholamines, and 2–3 weeks later for quantification of lipofuscin autofluorescence. Finally, these same tissues were treated with cresyl violet and photographed a third time to permit quantitative estimates of age changes in the number of Nissl staining Purkinje neurons. Electrophysiological studies revealed significant effects of age on a number of Purkinje cell firing parameters: in particular, increasing numbers of aberrant, very slow-firing cells were encountered in older animals. These cells showed normal climbing fiber mediated burst activity, but spontaneous simple spike firing rates 3–5 times less than normal. Rats exhibiting the highest numbers of such abnormal cells also exhibited the poorest Nissl staining. Conversely, good Nissl staining of Purkinje neurons in an old rat was a reliable predictor of relatively normal Purkinje cell firing. Lipofuscin was found to accumulate measurably in Purkinje neurons by 20 months of age, and to increase significantly thereafter. Deposition of the substance occurred almost exclusively at the apical pole of the soma. Our data suggest, however, that accumulation of lipofuscin in Purkinje neurons, as well as its reported accumulation in the inferior olive, is not a primary cause of electrophysiological dysfunction. There was no apparent age change in glyoxylic acid induced catecholamine fluorescence nor, in separate pharmacological studies, could any senescent alteration in cerebellar catecholamine levels be found.
DOI:
--
发表时间:
1992
期刊:
The Psychiatric clinics of North America
影响因子:
--
作者:
Fetner,HH;Geller,B
通讯作者:
Geller,B