Premium
Significance of Testosterone in Regulating Hypothalamic Content and In Vitro Release of β‐Endorphin and Dynorphin
Author(s) -
Almeida O. F. X.,
Nikolarakis K. E.,
Herz A.
Publication year - 1987
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1987.tb00956.x
Subject(s) - castration , medicine , endocrinology , dynorphin , opioid peptide , basal (medicine) , hypothalamus , testosterone (patch) , beta endorphin , hormone , chemistry , biology , opioid , receptor , insulin
The effects of castration and testosterone replacement on hypothalamic pools of β‐endorphin and dynorphin and on the basal and corticotropin‐releasing factor (CRF)‐stimulated release of these peptides from hypothalamic slices in vitro were studied. The experiments were done in adult male rats. The hypothalamic content of both peptides increased significantly within 1 week of castration, and levels remained elevated for up to 4 weeks. Testosterone treatment, begun at the time of castration, prevented these increases. In addition, testosterone replacement 6 weeks after castration reversed peptide levels to normal. Basal in vitro release rates of β‐endorphin and dynorphin were significantly lower from hypothalamic slices derived from 1‐week castrated animals than from intact males, and when testosterone was administered in various doses in vivo, basal release rates in vitro increased in a dose‐related manner. Hypothalami from rats that had been castrated for 4 weeks, however, showed basal release rates similar to those in tissues from intact controls, a finding indicating that castration initially alters both opioid peptide synthesis and release; later, release is normalized, whereas synthesis remains elevated. CRF was found to stimulate β‐endorphin and dynorphin release from hypothalami from intact and from 1‐ and 4‐week‐castrated rats, a result indicating that castration does not alter the response of β‐endorphin and dynorphin neurons to this stimulus.