The bovine preoptic area and median eminence: sites of opioid inhibition of luteinizing hormone-releasing hormone secretion.

Autoradiography was used to quantify opioid receptors in the median eminence (ME) and preoptic area (POA) of the brain of eight heifers, and in vitro perifusion of ME and POA tissue from seven cows and heifers was used to examine the release of LHRH after administration of naloxone (NAL). For quantitative receptor autoradiography, [3H]NAL was used as the radioligand and NAL or morphine as competitors. Specific binding of [3H]NAL in POA and ME resulted in linear Scatchard plots with similar equilibrium dissociation constants (Kd = 4.2 +/- 1.1 nM) and mean binding site densities in the POA and ME (POA: 80.3 +/- 5.8; ME 67.5 +/- 8.0 fmol/mm2). There were no differences between mean binding site densities of zonas externa and interna of the ME; however, between various regions of the POA within individual animals, binding site densities varied threefold (47.6 to 165.1 fmol/mm2). During in vitro perifusions of isolated POA and ME, basal LHRH secretion from ME decreased (P less than .001) from 15.9 +/- 1.8 to 7.3 +/- .8 pg/10 min fraction (500 microliters) but remained constant for POA (3.1 +/- .4 pg/fraction). Injections of medium alone did not affect LHRH secretion. Although there was no significant dose (10(-9) to 10(-7) M) effect, NAL increased (P less than .05) LHRH efflux from the ME and POA when administered at 110 min from the initiation of perfusion and again at 200 min for ME but not for POA. All tissues responded to KCl (30 mM) administered at 290 min of perifusion with increased (P less than .001) LHRH efflux. Both immunoreactive-LHRH and immunoreactive-beta-endorphin were immunocytochemically localized in neurons from some of these perifused tissues. We suggest that endogenous opioids suppress LHRH secretion by actions on specific opioid receptors located within the POA and ME of the brain.