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 recovery of visual behavioral function and of local cerebral glucose use (LCGU) has been observed. To evaluate whether this partial recovery of LCGU is due to a recovery of visual conductance (extrinsic) or intrinsic neuronal activity, visual stimulation alone and combined with physostigmine,an acetylcholinesterase inhibitor, were used to activate the retinofugal pathway. LCGU was determined in 30 male adult rats with or without physostigmine treatment 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. Furthermore, LCGU in the contralateral areas could not be stimulated by the treatment 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 visual input. We hypothesize a relief of an injury-dependent active suppression (diaschisis) of LCGU. This reversal of diaschisis may, in part, account for the return of visual functions after mild optic nerve injury.