作者: James W. Geddes , Michael C. Wilson , Freda D. Miller , Carl W. Cotman
DOI: 10.1007/978-1-4684-5769-8_47
关键词: Hippocampal formation 、 Granule cell 、 Kainic acid 、 Temporal lobe 、 Pathology 、 Synaptogenesis 、 Acetylcholinesterase 、 Epilepsy 、 Biology 、 Receptor
摘要: Reactive plasticity, including axonal and dendritic sprouting reactive synaptogenesis, has been proposed to contribute the pathogenesis of several neurological disorders. We have obtained evidence suggestive plasticity in Alzheimer’s disease temporal lobe epilepsy. In each these disorders, an altered distribution excitatory amino acid receptors, particularly kainic subtype, was observed hippocampal formation (Geddes et al., 1985; Cahan 1987; Geddes submitted). Altered binding sites also other forms childhood epilepsy (Represa 1989). Additional markers human disorders included intensification acetylcholinesterase staining 1985), supragranular Timm’s (Babb 1988). Although results are sprouting, this interpretation is open question. The increase receptor density could simply be result upregulation. from increased zinc existing terminals, relatively nonspecific. addition their lack specificity, many morphological methods used demonstrate rodent brain unsuitable for use postmortem tissue. For example, Timm requires perfusion with a sulfide solution optimal results.