Add time:07/21/2019         Source:sciencedirect.com

Neurons and glial cells are capable of synthesizing various bioactive steroids, but the neuronal mechanisms controlling neurosteroid-secreting cells are poorly understood. In the present study, we have investigated the possible effect of an endogenous ligand of benzodiazepine receptors, the triakontatetraneuropeptide (cas 120667-90-5) [17–50] (TTN), on steroid biosynthesis in the frog hypothalamus. Immunohistochemical studies revealed that most hypothalamic neurons expressing 3β-hydroxysteroid dehydrogenase/Δ5-Δ4-isomerase also contained peripheral-type benzodiazepine receptor-like immunoreactivity. Confocal laser scanning microscopic analysis revealed that the peripheral-type benzodiazepine receptor-immunoreactive material was located both in the cytoplasm and at the periphery of the cell bodies. By using the pulse-chase technique, TTN was found to stimulate the conversion of [3H]pregnenolone into various steroids, including 17-hydroxypregnenolone, 5α-dihydrotestosterone and 17-hydroxyprogesterone, in a dose-dependent manner. The peripheral-type benzodiazepine receptor agonist Ro5-4864 mimicked the stimulatory effect of TTN on the formation of neurosteroids. The peripheral-type benzodiazepine receptor antagonist PK11195 significantly reduced the effect of TTN on neurosteroid synthesis, while the central-type benzodiazepine receptor antagonist flumazenil did not affect the formation of neurosteroids evoked by TTN.These data indicate that TTN stimulates the biosynthesis of 3-keto-17α-hydroxysteroids in frog hypothalamic neurons through activation of peripheral-type benzodiazepine receptors likely located at the plasma membrane level.

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