A visuospatial dysfunction following posterior cortex injury is attenuated by postinjury administration of the ACTH4-9 analog ORG 2766.

Rats were trained in a Y-shaped water maze to discriminate a light gray from a medium gray visual stimulus. The latter stimulus card cued the location of a nonvisible escape platform. The animals received either a sham operation or a large ablation in the posterior neocortex, and osmotic minipumps were implanted subcutaneously in the animal's back. The pumps chronically administered either saline or ORG 2766 at a rate of 0, 1, or 10 micrograms per 24 h for 14 days while the animals recovered in individual rat cages. Four weeks after surgery retention of the discrimination was tested and, for those reattaining criterion, transposition of the habit to a pairing of the medium gray card with a black stimulus card was assessed. Animals treated with 10 micrograms ORG 2766 reattained criterion on the original discrimination more rapidly than did animals treated with 0 or 1 microgram. Neither the lesion nor the drug resulted in consistent influences upon transposition. There was no evidence that the drug protected neurons within the dorsal lateral geniculate nuclei. Postinjury treatment with some doses of ORG 2766 can attenuate the severity of some dysfunctions that accompany neurotrauma by influencing the development of behavioral compensation.