Opioid peptide inhibition of endogenous norepinephrine release from the A2 noradrenergic cell group in vitro.

We investigated the potential influence of opioid and melanotropic peptides on endogenous norepinephrine (NE) release from the A2 noradrenergic cell group of rats using a static, fixed-volume incubation procedure. Norepinephrine release from slices of caudal dorsomedial medulla (CDMM) was evoked by high potassium concentrations (20 and 60 mM) in a Ca(2+)-dependent and dose-related manner. Treatment with the potent melanotropin agonist [Nle4,D-Phe7] alpha-MSH(NDP-MSH) had no effect on K(+)-induced NE release. In contrast, human beta-endorphin1-31 significantly reduced K(+)-stimulated NE release, but not in the presence of naloxone. The highly-selective mu-opioid agonist [D-Ala2, N-Me-Phe4, Gly-ol5]-enkephalin (DAMGO) also significantly reduced evoked NE release. The inhibitory effect of DAMGO was completely blocked by naloxone. Naloxone alone did not alter evoked NE release. The inhibitory effect of DAMGO was not enhanced by reducing the stimulatory concentration of K+. None of the peptides tested influenced basal NE release. These data indicate that melanotropin receptors do not regulate NE release in CDMM. In contrast, the opioid peptides DAMGO and beta-endorphin inhibit K(+)-stimulated release of endogenous NE. These data suggest a role for mu-opioid receptors in controlling NE release from A2 noradrenergic neurons.

Diurnal variation in alpha-melanocyte-stimulating hormone content of various brain regions and plasma of the Texas toad, Bufo speciosus.

We measured the concentrations of alpha-melanocyte-stimulating hormone (alpha-MSH) in various brain regions as well as in the pituitary gland and plasma of the toad Bufo speciosus during a 24-hr light:dark cycle. There was significant diurnal variation of alpha-MSH concentrations in the hypothalamus and brainstem. In both areas alpha-MSH concentrations were highest during the scotophase. Peak alpha-MSH concentrations in the hypothalamus were observed at 21.00 and 05.00 hr, while a single peak in alpha-MSH concentrations was observed in the brainstem at 21.00 hr. In contrast, peak alpha-MSH concentrations in the plasma were observed during the photophase at 17.00 hr, when brain concentrations of alpha-MSH were low. There was no significant diurnal variation observed in the pituitary content of alpha-MSH throughout the 24-hr light:dark cycle. These data suggest that different mechanisms control hypothalamic and pituitary alpha-MSH cells in the toad during the 24-hr light:dark cycle. The fact that peak alpha-MSH concentrations were observed in the hypothalamus during the activity period of the toad is consistent with the proposed role of alpha-MSH peptides in learning and memory processes.