Electrical stimulation of the dorsal raphe nucleus (DRN) was administered to rats 2-4 weeks after ovariectomy and at least 7 days following implantation of a bipolar electrode. During stimulation the concentration of luteinizing hormone (LH) decreased whereas that of prolactin (Prl) increased in serial plasma samples obtained from the unanesthetized animals via a cannula chronically implanted in the right external jugular vein. Administration of estradiol benzoate (5 micrograms/100 g BW) for 2 days prior to the experiment reversed the effect of stimulation on LH but augmented the Prl response, suggesting modulation by estrogen of the relative effectiveness of opposing pathways ascending from DRN to influence LH release. It is also apparent that LH and Prl release are controlled by distinct mechanisms since estrogen exerted opposite influences on the responses of these two hormones to stimulation of DRN.
Effects of the serotonin receptor antagonists ketanserin, metergoline, and methysergide on LH release were tested in ovariectomized (OVX) rats pretreated with estradiol benzoate (EB) (5 micrograms/100 g BW) on each of the 2 days preceding the experiment. LH concentration measured by RIA in plasma samples obtained at 10 min intervals was analyzed using the PULSAR computer program to identify and characterize pulses observed in the LH profile of each rat individually. Multiple pulses were identified in seven of seven OVX rats but in only two of eight OVX rats primed with EB. Multiple pulses were identified in OVX EB-primed rats pretreated with ketanserin (six of seven), metergoline (three of seven), and methysergide (six of eight). Administration of the serotonin (5HT) agonist quipazine (2 mg/kg iv) to OVX rats inhibited pulsatile LH release and depressed mean plasma concentrations for approximately 45 min. This inhibitory response was antagonized by pretreatment of the OVX animals with ketanserin. These results suggest that 1) quipazine inhibits pulsatile LH release in OVX rats by a serotonin2 receptor mechanism; and 2) the inhibitory effect of estrogen on pulsatile LH release may also be mediated, at least in part, via 5HT2 systems.
We report studies of neurotransmitter and receptor species mediating the inhibition of LH release in ovariectomized (OVX) rats and stimulation in OVX estrogen-primed rats induced by electrical stimulation of the dorsal raphe nucleus (DRN). Attempts were made to block effects of stimulation of the DRN in groups of four to nine ovariectomized rats with or without priming with estradiol benzoate (EB) by pretreatment with the 5HT receptor antagonists ketanserin, methysergide, or metergoline; the alpha-adrenergic antagonist phenoxybenzamine; or the opiate antagonist naltrexone. Blood samples were collected via jugular cannulae from the unanesthetized rats at 10-min intervals before and during electrical stimulation of the DRN, and assayed by double antibody radioimmunoassay for LH. To test the effect of stimulation, data from animals in each treatment group were subjected to analysis of variance to obtain the contrast matrix including prestimulation and stimulation time points of interest. The contrast matrix was then used to construct an F ratio and thereby to evaluate the level of significance. In unprimed OVX rats the sustained decrease in plasma LH concentration during stimulation was prevented in rats pretreated with ketanserin or phenoxybenzamine. Methysergide pretreatment delayed the inhibitory effect of DRN electrical stimulation for 30 min, whereas metergoline and naltrexone were ineffective. In EB-primed animals the increase in plasma LH observed during stimulation was prevented in rats pretreated with metergoline, and reversed in those receiving naltrexone. Ketanserin limited the duration of the increase to 10 min, while phenoxybenzamine and methysergide had no significant effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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