Abstract

The role of noradrenaline (NA) and dopamine (DA) in the hypothalamic control of prolactin (PRL) secretion was investigated in hypothalamic intact (control) and hypothalamo-pituitary disconnected (HPD) Soay rams. The animals were exposed to alternating 16-weekly periods of short (8 L : 16D) and long days (16 L : 8D) to induce marked cyclical changes in PRL secretion in both groups (as demonstrated previously). Selective NA and DA receptor antagonists (dose: 1.2 micromol/kg) were administered under short days (low endogenous PRL secretion), and agonists (dose: 0.0012-0.12 micromol/kg) were administered under long days (high endogenous PRL secretion). The acute changes in blood PRL concentrations were measured over 4 h as the index of responsiveness. Under short days, treatment with WB4101 (alpha-1 adenoceptor antagonist), and rauwolscine (alpha-2 antagonist), consistently increased PRL secretion in control, but not in HPD rams. The treatments produced similar acute, drug-specific behavioural effects in both groups. Propranolol (beta antagonist) had no effect on PRL secretion, while sulpiride (DA D-2 antagonist) induced a marked increase in blood PRL concentrations in control rams (> 4 h), and a transient effect in HPD rams (15 min). Under long days, when endogenous PRL secretion was increased, phenylephrine (alpha-1 agonist) produced no effects, while bromocriptine (DA D-2 agonist) robustly decreased PRL concentrations in both control and HPD rams, even at the lowest treatment dose. Overall, the positive responses to the antagonists in the control rams, support the view that DA (acting via D-2 receptors), and to a lesser extent NA (acting via alpha-1/alpha-2 receptors), negatively regulate PRL secretion. In contrast, the lack of responses to the antagonists in the HPD rams, support the view that neither DA, nor NA, mediate the photoperiodic control of PRL secretion.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.