Opposite changes in the expression of enkephalin in the amygdala and hypothalamus after lesions of the bed nucleus of the stria terminalis in the rat.
The expression of enkephalin in neurons of the rat forebrain was studied by in situ hybridization and immunohistochemistry after unilateral injections of ibotenic acid into the bed nucleus of the stria terminalis. Initially, we observed that the destruction of nerve cell bodies in this nucleus resulted in a prominent bilateral increase in the number of neuronal perikarya immunoreactive for [Met]enkephalin in the lateral/basolateral amygdaloid complex-especially in the anterior division of the latter nucleus-as compared with NaCl-injected rats. In a separate set of experiments, this effect was associated with a significant (two times) enhancement of the number of nerve cell bodies containing preproenkephalin A messenger RNAs in the same amygdaloid nucleus ipsilateral to the injection, as compared with controls. In the hypothalamus of both experimental and control rats, the nerve cell bodies immunoreactive for [Met]enkephalin were few since the animals were not pretreated with colchicine, and the effects of the lesion were difficult to appreciate. However, using in situ hybridization, numerous nerve cell bodies containing preproenkephalin A messenger RNAs were detected bilaterally in the perifornical area, the paraventricular (parvocellular division) and the ventromedial nuclei of the hypothalamus. In the latter nucleus, the lesion of the bed nucleus of the stria terminalis resulted in a strong decrease (about two times) in the number of labelled cell bodies as compared with the controls, whereas no significant changes were found bilaterally in the paraventricular nucleus. In agreement with some data of the literature, our results indicate that the bed nucleus of the stria terminalis plays an important role in the regulation of neuropeptide genes expression in certain regions of the limbic system. Such a role is often exerted by nerve fibres afferents to the nerve cell bodies considered. However, from numerous neuroanatomical data of the literature, it appears more probable that the induction or inhibition of the expression of enkephalin in presynaptic neurons is due to the disappearance of their postsynaptic target in the bed nucleus of the stria terminalis.
Vankova
M
M
Université P. & M. Curie, CNRS (URA 1488), Dpt. Neurobiologie des Signaux Intercellulaires, Paris, France.
Boyer
P A
PA
Leviel
V
V
Arluison
M
M
D000679:Amygdala / Q000378:metabolism*; D000818:Animals; D004745:Enkephalins / Q000378:metabolism*; D007031:Hypothalamus / Q000378:metabolism*; D007051:Ibotenic Acid / Q000494:pharmacology; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008032:Limbic System / Q000187:drug effects / Q000502:physiology*; D008297:Male; D016548:Prosencephalon / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar
D004745:Enkephalins; D007051:Ibotenic Acid