4.5 Article

Densities of parvalbumin-immunoreactive neurons in non-malformed hippocampal sclerosis-temporal neocortex and in cortical dysplasias

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BRAIN RESEARCH BULLETIN
卷 68, 期 6, 页码 474-481

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PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.brainresbull.2005.10.008

关键词

epilepsy; cortical dysplasia; temporal lobe epilepsy; parvalbumin; inhibitory interneurons; neocortex

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The changes in density of inhibitory parvalbumin-immunoreactive internurons were quantitatively studied by immunohistochemistry in a series of human neocortical samples comprising the spectrum of malformations of cortical development (MCD) encountered in epilepsy surgery and the non-malformed hippocampal sclerosis-temporal neocortex in patients with refractory temporal lobe epilepsy. The highest relative density of parvalbumin-immumoreactive cells was obtained in the control samples (n=21). The number of parvalbumin-immunoreactive neurons was significantly decreased in non-malformed hippocampal sclerosis-temporal neocortex (n = 73, 80.5% of control values). In a proportion of the latter samples as well as in two controls we observed patchy regions of absence of parvalbumin staining. The total counts of parvalbumin-immunoreactive cells in all the categories of MCD - mild MCD (n = 25), focal cortical dysplasia type I (n = 19) and type 11 (it = 15) - were decreased representing 72.4%, 55.0% and 12.2% of control values, respectively. Significantly different parvalbumin-immunoreactive cell densities were demonstrated between the focal cortical dysplasia types IIA and IIB. In mild MCD, we observed a more pronounced decrease of parvalbumin-immunoreactive cells in the infragranular layers. No significant differences were revealed between the temporal and extratemporal examples of analogous MCD types. This study provides evidence for reduction of inhibitory parvalbumin-immunoreactive interneurons in the epileptic neocortex affected by MCD as well as in morphologically unaffected epileptic temporal neocortex, thus representing a possible mechanism for their epileptogenicity. (c) 2005 Elsevier Inc. All rights reserved.

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