Optokinetically evoked expression of corticotropin-releasing factor in inferior olivary neurons of rabbits

We investigated the influence of both binocular and monocular optokinetic stimulation on the expression of corticotropin-releasing factor (CRF), a neuropeptide, in inferior olivary neurons. Rabbits were placed at the center of a cylindrical optokinetic drum that rotated at a constant velocity of 5 degrees/sec, stimulating one eye in the posterior → anterior direction and the other eye in the anterior → posterior direction. After 48 hr of optokinetic stimulation, rabbits were killed and the brains were prepared for immunohistochemistry. An antiserum to rat/human CRF was used to label brainstem sections of optokinetically stimulated rabbits. The density of CRF- specific reaction product within individual olivary neurons was analyzed with a computer-based densitometer. Binocular optokinetic stimulation for 48 hr caused a 20-70% increase in the optical density of 'stimulated' dorsal cap neurons, measured relative to the optical density of control ('unstimulated') olivary neurons in the same histological section. This elevated expression of CRF lasted approximately 48 hr. When a delay of 18 hr was interposed between optokinetic stimulation and death of the rabbit, during which the rabbits were deprived of pattern vision, then both dorsal caps were densely labeled. Monocular optokinetic stimulation for 48 hr in the anterior → posterior direction caused no change in CRF expression in either dorsal cap if the rabbit was immediately killed. However, following monocular anterior → posterior stimulation, the dorsal cap contralateral to the 'null-stimulated' eye was densely labeled if the rabbit was deprived of pattern vision for 18 hr prior to death. We infer that stopping prolonged 'null stimulation' causes a rebound in activity in the stimulated dorsal cap. This 'rebound' must have its origin at the level of the dorsal cap or more peripherally in the optokinetic pathway.