Abstract
Progressive injury to the mammalian CNS often reduces the severity of lesion-induced deficits or spares the behavior from deficits altogether. The mechanism(s) underlying this behavioral sparing is not clearly understood, but axonal sprouting is a likely candidate. To test this possibility, unilateral, two-stage (progressive) lesions of the entorhinal cortex, which are known to accelerate sprouting by the crossed temporodentate pathway and spare spatial memory function, were made in rats. We examined the changes in synaptic efficacy (as measured by the amplitude and slope of evoked population EPSPs) of the crossed temporodentate projection after either one-stage or progressive unilateral lesions of the entorhinal area. Whereas the synaptic efficacy of the one-stage group did not differ significantly from the control group at 4, 6, or 8 d after the lesion, the synaptic efficacy of the crossed temporodentate pathway in the progressive lesion group significantly increased above the control values as early as 4 d after the lesion and remained stable thereafter. Axonal sprouting thus may provide a mechanism by which to account for behavioral sparing after progressive brain damage.