Functional Cerebral Activity during Regeneration from Entorhinal Lesions in the Rat

Abstract

Summary:The consequences of an unilateral electrolytic entorhinal lesion on the functional activity in all major anatomically defined brain regions were evaluated in the rat The '4C-2-deoxyglucose method served as a tool to quantify alterations of local cerebral glucose utilization (LCGU) ipsilateral and contralateral to the lesion at 4 days, 2 weeks, or 3 months after stereotaxic surgery, Apart from a few minor increases in the contralateral hemisphere, the predominant pattern consisted of reduc tions in the range of I�O% in the ipsilateral hemisphere, Ipsilaterally, in extrahippocampal areas, LCGU had re gained control levels at 2 weeks postlesion in contrast to hippocampal regions, where reductions were more proEntorhinal lesions have been employed in numer ous studies seeking to neurochemically characterize the processes governing the sprouting of new fibers in denervated hippocampal regions. It is well known that de-entorhination leads to a loss of �80-90% of synapses in the outer two-thirds of the mo lecular layer of the dentate gyrus, while the inner one-third remains largely unaffected, receiving its input mainly from commissural and associational fibers (Matthews et aI., 1976a). Though only driven by a denervation of <5%, the contralateral molec ular layer also initially exhibits synapse loss of 15% and subsequent replacement to control levels within months (Hoff et aI., 1981). Invariably, following creation of the lesions, massive sprouting occurs

Combined actions of Na+/K+-ATPase, NCX1 and glutamate dependent NMDA receptors in ischemic rat brain penumbra

“…There are many instances in which focal brain lesions also seem to have an impact on the function of surrounding or remote brain areas due to the fact that the brain can be considered as a network with multiple and intricate connections (Beck et al, 1996). Therefore, it is very important to analyze in detail which prognosis of focal cerebral ischemia is a direct consequence of the lesion, the perilesional area, or a reaction of the surrounding brain to the lesion.…”

Brain Glucose Hypometabolism after Perirhinal Lesions in Baboons: Implications for Alzheimer Disease and Aging

“…Unfortunately, a formal comparison of the duration of the hypometabolism induced by selective perirhinal damage and combined entorhinal-perirhinal lesion would be impossible, since the latest postlesion time point assessed in the latter study was 4.5 months. Despite these transient effects of perirhinal damage, which were also reported after entorhinal lesions in rats (Beck et al, 1996;Hayashi et al, 1999), it remains that the hypometabolic pattern detected at 4.5 months does not seem fortuitous, as discussed below.…”

t Progressive Unilateral Damage of the Entorhinal Cortex Enhances Synaptic Efficacy of the Crossed Entorhinal Afferent to Dentate Granule Cells

“…Under the conditions explored in our studies as well as related studies (L oesche and Steward, 1977;Reeves and Smith, 1987), the intact contralateral homolog of the injured cortex appears capable of supporting the lost functions occurring as a consequence of unilateral brain damage by virtue of lesion-induced axonal sprouting. Both current source density analysis (C lusmann et al, 1994) and 2-deoxyglucose metabolic assessment (Beck et al, 1996) of the reinnervated dentate gyrus raise the possibility that the reorganization fails to completely restore the dentate gyrus to normal electrophysiological and metabolic f unctioning, however. Despite these f unctional shortcomings, when taken together with our previous findings the present results show that the reorganized hippocampal formation regains a functional physiological capacity that enables it to ameliorate the consequences of memory impairments associated with cortical injury and hippocampal deafferentation.…”