Loss and subsequent recovery of local cerebral glucose use in visual targets after controlled optic nerve crush in adult rats.

A mild crush of the adult rat optic nerve serves as a model to study the restoration of function after traumatic brain injury. It causes a progressive degeneration of retinal ganglion cells, but visually guided behavior is partially restored within 2-3 weeks. The purpose of this study was to determine to what extent local cerebral glucose use (LCGU) decreases and if it recovers in retinofugal targets following unilateral optic nerve crush. At intervals of 2, 9, and 22 days after crush, LCGU was monitored in rats in which the visual system was stimulated by a strobe-light and pattern. In the ipsilateral retinofugal targets there was only a minimal loss of LCGU use, but in the contralateral retinofugal targets, LCGU was reduced at Postlesion Day 2: to 50% in the superior colliculus (SC), to 60% in the lateral geniculate nucleus of the thalamus (LGN), and to 87% in the visual cortex. On Postoperative Days 9 and 22 we observed a partial restoration of LCGU in the contralateral SC and LGN to 68 and 79%, respectively. As recovery of visual performance is known to follow a similar time course, we conclude that restoration of metabolic activity in target structures may contribute to the restoration of vision after optic nerve crush.