Fasting stimulates tuberoinfundibular dopaminergic neuronal activity and inhibits prolactin secretion in oestrogen-primed ovariectomized rats: involvement of orexin A and neuropeptide Y.
Fasting up-regulates central orexigenic systems including orexin A and neuropeptide Y (NPY) and it also inhibits the secretion of prolactin. We hypothesized that fasting may act through orexin A and NPY to influence tuberoinfundibular dopaminergic (TIDA) neurones, the major regulator of prolactin secretion. The effects of orexin A and NPY on TIDA neuronal activity and prolactin secretion were determined in oestrogen-primed ovariectomized rats, and the effects of fasting and the involvement of orexin A and NPY were tested. Orexin A, NPY and its analogs were administered through preimplanted intracerebroventricular (i.c.v.) cannulae. TIDA neuronal activity was determined by measuring concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) or 3,4-dihydroxyphenylalanine in the median eminence. i.c.v. injection of NPY (10 microg) or orexin A (1 microg) concomitantly increased median eminence DOPAC and decreased serum prolactin concentrations. The effect of NPY was mimicked by a Y1 receptor agonist at lower doses (0.1 and 1 microg) and no additive effect was observed when orexin A and the Y1 agaonist were coadministered. Moreover, a Y1 receptor antagonist, BIBP, not only blocked the effect of Y1 agaonist, but also that of orexin A. Treatment with BIBP alone decreased median eminence DOPAC and increased serum prolactin concentrations, indicating that endogenous NPY may play a role. Moreover, fasting for 48 h significantly increased TIDA neuronal activity, both in the morning and afternoon, and the effect was reversed by treatment with either BIBP or an antibody against orexin A. The findings support our hypothesis that fasting stimulates TIDA neuronal activity and inhibits prolactin secretion through up-regulated central orexin A and NPY systems.
Hsueh
Y-C
YC
Department of Physiology, School of Life Science, National Yang-Ming University, Taipei, Taiwan.
Cheng
S-M
SM
Pan
J-T
JT
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D002352:Carrier Proteins / Q000494:pharmacology*; D004298:Dopamine / Q000502:physiology; D004967:Estrogens / Q000494:pharmacology; D005215:Fasting / Q000502:physiology*; D005260:Female; D047908:Intracellular Signaling Peptides and Proteins; D008473:Median Eminence / Q000166:cytology / Q000378:metabolism / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D009478:Neuropeptide Y / Q000031:analogs & derivatives* / Q000378:metabolism / Q000494:pharmacology*; D009479:Neuropeptides / Q000494:pharmacology*; D064446:Orexin Receptors; D000068797:Orexins; D010052:Ovariectomy; D010904:Pituitary Gland, Posterior / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D043562:Receptors, G-Protein-Coupled; D018013:Receptors, Neuropeptide; D017476:Receptors, Neuropeptide Y / Q000819:agonists / Q000378:metabolism
D002352:Carrier Proteins; D004967:Estrogens; D047908:Intracellular Signaling Peptides and Proteins; D009478:Neuropeptide Y; D009479:Neuropeptides; D064446:Orexin Receptors; D000068797:Orexins; D043562:Receptors, G-Protein-Coupled; D018013:Receptors, Neuropeptide; D017476:Receptors, Neuropeptide Y; C097212:neuropeptide Y-Y1 receptor; D015102:3,4-Dihydroxyphenylacetic Acid; C062259:neuropeptide Y, Leu(31)-Pro(34)-; D011388:Prolactin; D004298:Dopamine