Devascularizing Injury of the Rat Brain Neocortex Causes Different Neurotrophic Responses in Denervated Nucleus Basalis Magnocellularis and Thalamic Nuclei

摘要: Cerebral infarction in man (1) and experimental animals (2–10) leads to functional pathological alterations brain regions directly affected by ischemia areas remote from the infarct. In a model of permanent cerebral caused partial removal pia-arachnoid vasculature, number time-dependent events affecting cortex subcortical structures occurs (5,6,9,10). A retrograde degeneration two major corticopetal systems develops: (a) that nucleus basalis magnocellularis (NBM), providing main cholinergic input cortex, (b) other, thalamic nuclei, provides specific sensory projections relay neurons (7,8). These differ vulnerability lesion-caused damage their cortical terminals: multiple laterodorsal (LD) ventroposterior (VP) nuclei undergo cell death (4,7,8), while NBM shrink, but do not die (5,6). The causes an extreme sensitivity axotomy remain obscure; one them may be limited responsiveness endogenous trophic activity. uninjured brain, expression neurotrophins receptors (11,12). After injury, sustain nerve growth factor (NGF), require NGF treatment rescue atrophy dysfunction Data on postinjury activity are lacking. However, it was shown these prevented CNTF administration (13). While action is exerted responsive neurons, effect thalamus suggested mediated through glial cells (14). That some reactive astroglia gain capacity express neurotrophin after trauma were re-cently several investigators, including our laboratory (15,16). Devascularizing lesion extensive astrogliosis (7,8,9); there no data astroglial response. Thus studies neuronal non-neuronal following devascularization offer clues mechanisms lead detrimental beneficial cells. this study we present part immunocytochemical postlesion (NGF high-affinity receptor (TrkA)) NBM, glia.