Schallert T, Jones T A, Lindner M D
Department of Psychology, University of Texas, Austin 78712.
Stroke. 1990 Nov;21(11 Suppl):III143-6.
Recent morphologic and behavioral studies of the effects of gamma-aminobutyric acid agents on transsynaptic degeneration after cortical and striatal damage are reviewed and discussed. Following unilateral lesions of the anteromedial cortex, mild atrophy appears in the ipsilateral striatum and substantia nigra pars reticulata. Long-term diazepam administration greatly enhances this degeneration, extends the degeneration into the thalamus, and severely disrupts recovery from somatosensory asymmetries. Following unilateral excitotoxic lesions of the striatum, progressive degeneration of neurons occurs in the substantia nigra pars reticulata and efferent targets in the thalamus. This degeneration can be prevented by chronic infusion of muscimol, a gamma-aminobutyric acid agonist. Unexpectedly, this treatment did not facilitate recovery from somatosensory asymmetries. Recovery in muscimol-treated animals was impaired relative to saline-treated controls. Thus, gamma-aminobutyric acid agonists either may enhance or prevent neural atrophy secondary to brain damage, but the behavioral outcome appears to depend importantly on the excitatory and inhibitory characteristics of the affected networks.
本文回顾并讨论了近期关于γ-氨基丁酸制剂对皮质和纹状体损伤后跨突触变性影响的形态学和行为学研究。在前内侧皮质单侧损伤后，同侧纹状体和黑质网状部会出现轻度萎缩。长期给予地西泮会极大地加剧这种变性，使变性扩展至丘脑，并严重干扰体感不对称的恢复。在纹状体单侧兴奋性毒性损伤后，黑质网状部的神经元以及丘脑的传出靶点会发生进行性变性。这种变性可通过长期输注γ-氨基丁酸激动剂蝇蕈醇来预防。出乎意料的是，这种治疗并未促进体感不对称的恢复。与生理盐水处理的对照组相比，接受蝇蕈醇治疗的动物的恢复受损。因此，γ-氨基丁酸激动剂可能会增强或预防继发于脑损伤的神经萎缩，但行为结果似乎在很大程度上取决于受影响网络的兴奋和抑制特性。
