Prolonged c-Jun expression in the basolateral amygdala following bulbectomy: possible implications for antidepressant activity and time of onset

Olfactory bulbectomy is a well established animal model of depression. Neur ochemical and behavioral alterations observed following olfactory bulbectom y. are due, in part, to the neurodegeneration of specific brain structures. Amygdaloid dysfunction in particular, is known to play a substantial role in the syndrome of the olfactory bulbectomized rat. The present study exami ned both short- and long-term alterations in immediate early gene expressio n, tyrosine hydroxylase and serotonin immunoreactivity, and classical silve r staining, following olfactory bulbectomy in the basolateral amygdala. The results indicated no consistent change in Fos expression observed over the experimental period. Following bulbectomy, long term (up to 64 days post-l esion) Jun expression, not coincident with silver staining, was observed in the basolateral nucleus. The basolateral nucleus was also intensely immuno reactive for serotonin at this timepoint post-bulbectomy. Thus, following b ulbectomy long term alterations in Jun expression occurs in the serotonin r ich basolateral amygdala. As a site of action fur antidepressant compounds, alterations at the immediate early gene level in this region may have impl ications both for the model, and antidepressant drug action therein. (C) 20 00 Elsevier Science B.V. All rights reserved.