THE ROLE OF CALCITONIN GENE-RELATED PEPTIDE IN THE CONTROL OF GROWTH-HORMONE AND PROLACTIN-RELEASE

In order to evaluate the actions of calcitonin gene-related peptide (CGRP), a neuropeptide which is found within the hypothalamus, male and ovariectomized (OVX)female rats were injected intraventricularly (third ventricle. 3V) with varying doses of CGRP or antiserum directed against the peptide and the effect on plasma growth hormone (GH) and prolactin (Prl) concentrations studied. Intraventricular injection of the peptide (0.5 or 5.0 µg; 0.125 or 1.25 nmol)induced a suppression ofGH release in conscious, OVX female and intact male rats. Conversely, intraventricular injection of diluted (1:10) highly specific antiserum against the peptide produced the reverse effect and a transient elevation in plasma GH occurring 2 h after the injection in males. A longer-lasting elevation occurred in OVX females which persisted for the 24-hour duration of the experiment. The elevation was delayed as has been the case with other antisera suggesting that the site of action was at some distance from the site of injection into the 3V. Since the peptide had an action to inhibit GH release from dispersed, overnight cultured anterior pituitary cells in vitro at doses of 10-11 it is not certain from these results whether or not the effects of the peptide are exerted directly on the hypothalamus or the pituitary, but the results indicate a physiologically significant action of this peptide to suppress GH release. Similarly, intraventricular injection of the peptide produced a dose-related suppression of Prl release in OVX animals; however, antiserum directed against the peptide failed to alter Prl release. In males, only the lower 0.5µg dose effectively inhibited Prl release. There was an action of the peptide to increase Prl release by dispersed cells in vitro. Therefore, the suppressive effect of the peptide on Prl release following its intraventricular injection must be exerted on the hypothalamus to either augment the release of Prl-inhibiting factors or suppress the release of Prl-releasing factors. This action does not appear to be physiologically significant in the types of animals tested since the antiserum had no effect. © 1990 S. Karger AG, Basel.