Effects of Intraventricular Catecholamines on Luteinizing Hormone Release in Ovariectomized-Steroid-Primed Rats

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Abstract
The effects of intraventricular norepinephrine (NE) and dopamine (DA) were studied in the awake, freely behaving rat. In long-term ovariectomized, estrogen-progesterone-primed (OVX E2-P) animals, blood samples were taken via indwelling intra-atrial catheters before and after intraventricular infusion of either pH-adjusted saline, NE (5 .mu.g, 15 .mu.g, 20 .mu.g) or DA (4 .mu.g, 15 .mu.g), and plasma LH [luteinizing hormone] was measured by radioimmunoassay. Under urethane anesthesia, records were made of the effects of intraventricular saline and NE on the electrical activity of the arcuate nucleus in the form of multi-unit spike activity. In unanesthetized animals intraventricular NE markedly changed behavior. The typical response consisted of 3 phases: generalized activation (5-7 min), feeding (5-15 min) and sleep (1-2 h), DA exerted similar behavioral effects but without the marked sleep phase characteristic of the NE response. The effects of the catecholamines on LH output were significant increases in plasma LH levels for all NE doses tested (5 .mu.g, P < .025; 15 .mu.g, P < .05; 20 .mu.g, P < .005) while DA had no effect. The dynamics of the LH response to NE were similar at all dosage levels, and the increase caused by 20 .mu.g NE was essentially equal to that induced by a quick i.v. infusion of 1.25 ng LHRH [luteinizing hormone-releasing hormone]. Arcuate nucleus multi-unit spike activity (MUSA) showed a clear response to intraventricular NE at a dosage capable of stimulating the release of LH. In every case the initial effect was a decrease in spike activity. These results, considered in relation to previous findings, suggest that NE may be stimulatory to neurons secreting LH-releasing hormone (LHRH). The decrease in arcuate nucleus MUSA in response to NE implies that certain elements of this nucleus are inhibited during LH release, perhaps the dopaminergic tuberoinfundibular neurons.