ISSN:
1365-2826
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Met-enkephalin and β-endorphin induced a partial reversion of the dopamine inhibition of prolactin release from pituitary cells of lactating rats in primary culture. This effect of opiate peptides was dose-dependent with an EC50 of 40 ± 8 nM and 45 ± 7 nM and maximal blockade of dopamine inhibition of 60% and 68% for Met-enkephalin and β-endorphin, respectively. Naloxone antagonized the effect of Met-enkephalin with an EC50 of 22 ± 12 nM. Furthermore, this Met-enkephalin effect on dopamine inhibition of prolactin secretion appeared non-competitive since it reduced maximal inhibition without affecting the apparent affinity of dopamine. Finally, it should be noted that the two opiate peptides had no effect on spontaneous prolactin release.In electrophysiological experiments, local ejection of dopamine on tested cells induced an hyperpolarization concomitant with an increase of the membrane conductance. Ejection of Met-enkephalin or β-endorphin alone did not modify the electrical properties of the cells (resting potential, membrane conductance and excitability). In contrast, both peptides blocked in a reversible manner the dopamine-induced electrical responses. These effects were antagonized by naloxone. However, this interaction of opiatepeptides with dopamine electrical response was not observed on all cells tested. We conclude that the blocking effect of opiates on dopamine-induced hyperpolarization may account, at least in part, for the ability of these peptides to interact with dopamine inhibition of prolactin release.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1365-2826.1990.tb00645.x
