PROLACTIN SECRETION IN FEMALE SIBERIAN HAMSTERS FOLLOWING HYPOTHALAMIC DEAFFERENTATION - ROLE OF PHOTOPERIOD AND DOPAMINE

The role of the hypothalamic paraventricular nucleus (PVN) region in t he control of seasonal prolactin (PRL) responses was investigated in f emale Siberian hamsters via disruption of PVN afferent connections fro m the region of the suprachiasmatic nucleus (SCN). Adult female hamste rs received sham surgery or horizontal knife cuts placed ventral to th e PVN so as to sever dorsally projecting fibers from the SCN and were either immediately transferred to a short-day photoperiod [10 h light: 14 h dark(10L:14D); experiment (exp.) 1A] or returned to the long-day photoperiod (16L:8D; exp. 1B and 2). Serial blood samples were analyze d for determination of circulating PRL and follicle-stimulating hormon e (FSH; exp. 1A)levels at various time points after surgery. In exp. 1 A, sham-operated animals showed a steady decline in circulating levels of both PRL and FSH during exposure to 10L. Animals with knife cuts t hat passed through the extent of the SCN were prevented from showing d eclines in PRL and FSH during exposure to 10L. Animals with knife cuts located ventral to or through the PVN but dorsal to the SCN maintaine d high FSH levels during short-day exposure but showed a decline in PR L. Similarly, animals with knife cuts in exp. 1B and 2 showed a declin e in circulating PRL despite continued exposure to a stimulatory photo period. In exp. 2, the efficacy of a dopaminergic agonist (CB154) and an antagonist (pimozide) in altering circulating PRL under the 16L pho toperiod was evaluated. CB154 induced declines in PRL in knife-cut but not sham-operated animals, whereas administration of pimozide elevate d circulating PRL in both groups. These results suggest that disruptio n of afferent input to the PVN region may result in reductions in circ ulating PRL independently of the photoperiodic regulation of this horm one, and via mechanisms other than increased dopaminergic tone, i.e., possibly through disruption of a hypothalamic PRL-stimulating system.