Brain ACTH and endorphin reduced in rats with monosodium glutamate-induced arcuate nuclear lesions

Abstract

IMMUNOASSAY and immunocytochemical techniques, in some instances with additional characterisation by bioassay and gel filtration, have demonstrated the presence of ACTH-like^1–10, β-lipotropin (LPH)-like^{6,8,9,11–13} and beta-endorphin-like^6,14,15 activity within the central nervous system. However, the source of these peptides in the central nervous system is uncertain³. Hypophysectomy is not associated with any change in hypothalamic content of ACTH^1,5,10 or of beta-endorphin-like material¹⁴, suggesting a non-pituitary, presumably central nervous system, origin. Immunoreactive perikarya containing ACTH-like^8–10,16,17, β-LPH-like^{8,9,11,13,16,17} and β-endorphin-like^15–17 material have thus far only been demonstrated in the arcuate nucleus and adjacent lateral areas of the mediobasal hypothalamus. We considered that if the arcuate nucleus were the source of ACTH-like activity within other areas of the central nervous system, its destruction would result in a decrease of such activity. Neonatal administration of sodium glutamate produces central nervous system lesions, restricted largely to neurones of the arcuate nucleus and to the retina¹⁸, while sparing fibres of passage¹⁹. We report here that, using neonatal sodium glutamate administration to produce such arcuate nucleus destruction in rats, the content of ACTH and β-endorphin-like material in the hypothalamus and other brain regions is markedly reduced in the absence of any change in whole pituitary, anterior lobe or plasma ACTH concentrations.