DEAFFERENTATION REMOVES CALRETININ IMMUNOPOSITIVE TERMINALS, BUT DOESNOT INDUCE DEGENERATION OF CALBINDIN D-28K AND PARVALBUMIN EXPRESSINGNEURONS IN THE HIPPOCAMPUS OF ADULT-RATS

Unilateral combined transections of the fimbria-fornix and angular bun dle in adult Fischer 344 rats were used to study the effects of deaffe rentation on hippocampal expression of calretinin, calbindin D-28k, an d parvalbumin. Reflecting the widespread degeneration of synaptic cont acts, immunostaining for glial fibrillary acidic protein 6 days after the lesions was increased in lacunosum-molecular and oriens layers of CA1, 2, and 3 in ipsi- and contralateral hippocampus and in the ipsila teral dentate gyrus outer molecular layer. At 21 days the immunoreacti vity had decreased to control levels except for a still slightly incre ased signal in the oriens layer of CA1-3. At 6 and 21 days after the c ombined lesions the numbers of hippocampal neurons containing calretin in, parvalbumin, and calbindin D-28k was unaltered. The combined lesio ns abolished calretinin containing terminals in the dentate gyrus inne r molecular layer on the deafferentated side. This could be reproduced by single unilateral fimbria-fornix transections, suggesting that the axons of these calretinin positive terminals project to the hippocamp us through the fimbria-fornix. The most likely origin of the calretini n positive terminals are neurons in the supramammillary hypothalamic n ucleus. Our findings demonstrate that the extensive lesion-induced syn aptic rearrangements in the adult hippocampus do not induce degenerati on of hippocampal neurons expressing calretinin, calbindin D-28k, and parvalbumin, but do remove calretinin containing terminals which reach their targets in the hippocampus through the fimbria-fornix. (C) 1994 Wiley-Liss, Inc.