Prolactin activates all three populations of hypothalamic neuroendocrine dopaminergic neurons in ovariectomized rats

Prior studies suggest that prolactin (PRL) stimulates release of dopamine ( DA) from tuberoinfundibular dopaminergic (TIDA) neurons. In the present stu dy, the time course over which PRL exerts its effects on all three populati ons of neuroendocrine dopaminergic (DAergic) neuron populations [TIDA, tube rohypophyseal (THDA) and periventricular-hypophyseal (PHDA)] was determined . Ten days following ovariectomy (OVX), groups of female rats were injected either with 15 mu g of ovine PRL (oPRL) or saline at 0900 h. Rats were dec apitated every 30 min from 0830 h-1100 h and hourly from 1200 h-1500 h. Tru nk blood was assayed for rat PRL (rPRL) and oPRL using species-specific rad ioimmunoassays (RIAs). The concentration of DA and 3,4-dihydroxyphenylaceti c acid (DOPAC) in the median eminence (ME), as well as the anterior (AL), i ntermediate (IL) and neural (NL) lobes of the pituitary gland were determin ed by HPLC-EC. The concentration of rPRL in oPRL-treated animals, compared to saline-treated animals, was diminished by 1000 h and again between 1200 h-I500 h. DOPAC/DA ratio, an indicator of dopaminergic neuronal activity, i ncreased spontaneously in the ME, IL, and NL during the afternoon in OVX ra ts. In animals injected with oPRL at 0900 h, the DOPAC/DA ratio increased i n the ME, IL and NL within 1 h. Moreover, a secondary increase in the DOPAC /DA ratio in the IL and NL occurred during the afternoon in oPRL-treated ra ts. However, the second increase of DA turnover present in the ME of contro l animals never occured in oPRL-treated animals. Furthermore, there were tw o increases in the concentration of DA in the AL: the first coincided with the increased turnover of DA in all three terminal areas and the second wit h increased DA turnover in the IL and NL. These data suggest that all three populations of hypothalamic neuroendocrine DAergic neurons are activated b y PRL and that PHDA/THDA neurons have a second 'delayed' activation. (C) 19 99 Elsevier Science B.V. All rights reserved.