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 (MBH) with nor-binaltorphimine (nor-BNI) stimulates luteinizing hormone (LH) release during midpregnancy in the rat [48]. The objective of this 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 monitor in vivo NE release in the MBH occurring in response to (a) artificial CSF followed by CSF containing nor-BNI (40 micrograms/h), (b) desipramine (DMI, a NE reuptake blocker, 10 microM) 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 levels were determined by RIA. Nor-BNI significantly increased LH release compared to CSF alone, but perfusate NE was undetectable in either perfusion period. However, perfusion with CSF containing 100 mM K+ in these rats markedly increased perfusate NE levels, indicating noradrenergic nerve terminals were present at the perfusion sites in the MBH. Addition of DMI to the CSF significantly increased perfusate NE levels, but produced no change in LH release. Nor-BNI+DMI perfusion increased LH secretion similar to nor-BNI alone, but produced no additional increase in MBH perfusate NE levels compared to perfusion with DMI alone.(ABSTRACT TRUNCATED AT 250 WORDS)