LACK OF CATECHOLAMINE INVOLVEMENT IN THE INCREASED LUTEINIZING-HORMONE RELEASE DUE TO BLOCKADE OF KAPPA-OPIOID RECEPTORS IN THE MEDIAL BASAL HYPOTHALAMUS DURING MIDPREGNANCY IN THE RAT

Blockade of kappa-opioid receptors in the medial basal hypothalamus (M BH) with nor-binaltorphimine (nor-BNI) stimulates luteinizing hormone (LH) release during midpregnancy in the rat [48]. The objective of thi s study was to determine whether norepinephrine (NE) or dopamine (DA) mediates the LH response to blockade of MBH kappa-opioid receptors on days 13-17 of pregnancy in the rat. Two experiments were conducted. In the first, push-pull perfusion in conjunction with HPLC was used to m onitor in vivo NE release in the MBH occurring in response to (a) arti ficial CSF followed by CSF containing nor-BNI (40 mu g/h), (b) desipra mine (DMI, a NE reuptake blocker, 10 mu M) in CSF followed by DMI, and (c) DMI followed by DMI + nor-BNI. Blood samples were taken at 12 min intervals concurrent with push-pull perfusate samples. Plasma LH leve ls were determined by RIA. Nor-BNI significantly increased LH release compared to CSF alone, but perfusate NE was undetectable in either per fusion period. However, perfusion with CSF containing 100 mM K+ in the se rats markedly increased perfusate NE levels, indicating noradrenerg ic nerve terminals were present at the perfusion sites in the MBH. Add ition of DMI to the CSF significantly increased perfusate NE levels, b ut produced no change in LH release. Nor-BNI + DMI perfusion increased LH secretion similar to nor-BNI alone, but produced no additional inc rease in MBH perfusate NE levels compared to perfusion with DMI alone. In the second experiment, push-pull perfusion in the MBH with nor-BNI was done in rats pretreated either with the NE synthesis inhibitor FL A-63 (25 mg/kg, s.c.), the alpha-adrenergic receptor blocker phentolam ine (5 mg/kg, i.v.), the DA receptor antagonist d-butaclamol (1 mg/kg, s.c.), or vehicle. None of these drug treatments affected the increas ed LH release occurring during MBH perfusion with nor-BNI. The present results demonstrate that neither NE nor DA mediates the increased LH release occurring in response to blockade of kappa-opioid receptors in the MBH during midpregnancy in the rat.