PROLACTIN-INDUCED AND TESTOSTERONE-INDUCED INHIBITION OF LH-SECRETIONAFTER ORCHIECTOMY - ROLE OF CATECHOLAMINERGIC NEURONS TERMINATING IN THE DIAGONAL BAND OF BROCA, MEDIAL PREOPTIC NUCLEUS AND MEDIAN-EMINENCE

Central catecholaminergic neurones projecting to specific hypothalamic structures are involved in stimulating and inhibiting the, activity o f the GnRH-containing neurosecretory neurones. Both testosterone and e levated circulating prolactin (PRL) levels inhibit postcastration LH r elease. Three groups of adult male rats were orchidectomized and adren alectomized, received corticosterone replacement and were: (i) adminis tered purified ovine PRL (oPRL; 2400 mu g/s.c. injection) or (ii) its diluent, polyvinylpyrrolidone (PVP), every 12 h, or (iii) received phy siological testosterone replacement for 2 days. At 0, 2 and 6 days pos tcastration, norepinephrine (NE), epinephrine (E) and dopamine (DA) tu rnover were estimated by the alpha-methyl-p-tyrosine method in three m icrodissected hypothalamic structures: the diagonal band of Broca at t he level of the organum vasculosum of the lamina terminalis (DBB(ovlt) ), the medial preoptic nucleus (MPN) and the median eminence (ME). In control (PVP-treated) rats, serum LH concentrations increased eightfol d at 2 and 6 days postcastration and this rise was prevented by testos terone. oPRL treatment transiently suppressed LH secretion at 2 but no t 6 days postcastration. Castration significantly decreased basal rat PRL (rPRL) levels at 2 and 6 days and testosterone administration part ially prevented this effect. NE turnover in the ME and E turnover in t he MPN increased markedly at 2 and 6 days postcastration, and testoste rone replacement for 2 days prevented these increases. Thus, noradrene rgic neurones innervating the ME and adrenergic neurones innvervating the MPN may drive postcastration LH secretion by providing stimulatory afferent input to the GnRH neurones. It was striking to observe that oPRL blocked the increases in both ME NE and MPN E turnover at 2 but n ot 6 days postcastration. Hence, oPRL may transiently suppress LH rele ase by an inhibitory action on these NE and E neurones. DA turnover in the DBB(ovlt) was significantly decreased by 6 days postcastration. T estosterone-treated (2 days postcastration) and oPRL-treated (2 and 6 days postcastration) rats exhibited turnover values indistinguishable from day 0 controls. Hence, the A(14) dopaminergic neurones, which syn apse on GnRH neurones in the rostral preoptic area and may exert an in hibitory effect on them, are positively regulated by PRL and perhaps b y testosterone as well. Autoregulatory feedback suppression of endogen ous rPRL secretion by oPRL was observed both 2 and 6 days postcastrati on. In contrast to the A(14) dopaminergic neurones, turnover in the A( 12) tuberoinfundibular dopaminergic (TIDA) neurones innervating the ME increased significantly by 6 days postcastration in control rats whil e oPRL administration further increased ME DA turnover at both 2 and 6 days. Hence, autofeedback regulation of rPRL secretion persists throu gh at least 6 days of oPRL exposure temporally associated with markedl y increased turnover in the TIDA neurones. In summary, our results sup port the hypothesis that the inhibitory effect of PRL on postcastratio n LH release is mediated by suppression of the activity of NE neurones innervating the ME and E neurones terminating in the MPN which, with time, become refractory to continued PRL exposure.