Recovery of pulsatile luteinizing hormone secretion following permanent disruption of the ascending noradrenergic fiber tract in the ovariectomized rat.

Abstract

To determine whether noradrenergic (NE) support was essential for the generation of pulsatile luteinizing hormone (LH) secretion, we studied the effect of acute and chronic disruption of central noradrenergic pathways on patterns of LH release in the ovariectomized female rat. We argued that if NE pathways were essential for the generation of pulsatile LH secretion, then disruption of central NE activity should effect a blockade of LH pulses. To test this hypothesis we chronically disrupted NE activity by transecting the ascending NE pathway (ANP) and acutely disrupted NE activity by administering the alpha-adrenergic receptor blocking agent phenoxybenzamine (PBZ); and we evaluated the effect of these treatments on the pattern of pulsatile LH secretion. Four weeks after the ANP transections, we found no differences in either LH pulse amplitude or frequency between ANP-cut animals (n = 6) and sham-cut controls (n = 8). In sham-cut animals (n = 7), PBZ reduced LH pulse frequency by 85% (P less than 0.002) and had no effect on pulse amplitude. In contrast, PBZ was significantly less effective in reducing LH pulse frequency in ANP- cut rats (n = 9); pulse frequency in these animals was 4 times greater than that found in PBZ-treated, sham-cut rats. We conclude from these data that, whereas noradrenergic pathways usually interact with LH regulatory mechanisms, they are not essential for the generation of normal gonadotropin-releasing hormone pulses.