Recovery of metabolic activity in retinofugal targets after traumatic optic nerve injury is independent of retinofugal input

Traumatic injury of the adult optic nerve causes a progressive degeneration of retinal ganglion cells. Despite this ongoing degeneration, a partial re covery of visual behavioral function and of local cerebral glucose use (LCG U) has been observed, To evaluate whether this partial recovery of LCGU is due to a recovery of visual conductance (extrinsic) or intrinsic neuronal a ctivity, visual stimulation alone and combined with physostigmine, an acety lcholinesterase inhibitor, were used to activate the retinofugal pathway. L CGU was determined in 30 male adult rats with or without physostigmine trea tment 2 or 9 days after crush or 8 days after cut of the right optic nerve. Analysis of LCGU in contralateral first-order projection areas revealed no differences 8 days after cut and 9 days after optic nerve crush. Furthermo re, LCGU in the contralateral areas could not be stimulated by the treatmen t with physostigmine. We therefore conclude that the increase in LCGU from 2 to 9 days after crush is not due to a recovery in the conductance of visu al input. We hypothesize a relief of an injury-dependent active suppression (diaschisis) of LCGU. This reversal of diaschisis may, in part, account fo r the return of visual functions after mild optic nerve injury.