Median Raphe Stimulation and Sham Procedures Inhibit the LH Surge

Abstract

Acute electrolytic stimulation of the median raphe (MR) nucleus (MR Stim) between 13:00 and 16:00 h on proestrus blocked ovulation in 10 of the 21 rats tested, whereas all sham-treated (MR Sham, no current) animals ovulated normally (n = 12). MR Stim at 16:00 h on proestrus in individual cannulated rats ‘turned off’ the luteinizing hormone (LH) surge in all animals tested. Unexpectedly, MR Sham treatment also abruptly inhibited the LH surge, although all animals ovulated. Manipulations associated with acute surgical procedures (puncture of the dura mater, ether anesthesia alone) were also found to inhibit the LH surge, with the magnitude of LH inhibition directly related to the severity of the operative procedures performed (p< 0.025). The results suggest (1) that inhibition of ovulation following MR stimulation can be attributed to a response to stress qualitatively similar but more severe than that experienced by the MR sham group, and (2) that inhibitory inputs to the ovulatory LH release mechanism cannot be studied using acute surgical procedures.

Inhibition of Proestrous LH Surge and Ovulation in Rats Evoked by Stimulation of the Medial Raphe Nucleus Involves a GABA-Mediated Mechanism

“…The ability of electrochemical stimulation of the MRn to in hibit the preovulatory surge of LH and ovulation observed in the present work is in agreement with previously reported re sults [5,8,33,52], These findings suggest that activation of MRn neurons inhibits the release of LH on the day of proest rus. That this effect is due to the activation of a serotonergic pathway is supported by several facts, namely: (a) the MRn is rich in neurons that contain and synthezise 5-HT (12,53] and send ascending axons to the preoptic area-medial basal hypo thalamus [2,3,11,32,38,43,54]; (b) local injections of the 5-HT synthesis inhibitor, /;-chlorophenylalanine (PCPA), pre vented the inhibitory effect of MRn stimulation on LH release [33]; (c) systemic injection of the 5-HT antagonist, methyser gide, in the present work also prevented the inhibition of LH release evoked by MRn stimulation; and (d) lesions in the MRn produced a significant decrease of 5-HT content [21,27] and tryptophan hydroxylase activity [18,23] in the hypothalamus, and electrochemical stimulation of this nucleus has been shown to produce an increase in multiunit spike activity in the medial preoptic area [7].…”

Involvement of the Preoptic Region in Gonadotropin Release-Inhibition in Goldfish, <i>Carassius auratus</i>

“…In spite of these reports a physiological function for a GRIF has not been proposed for mammals. Inhibitory influences from the telencephalon on LH-releasing mechanisms have been demonstrated by lesioning [9], Electrical stimulation of the midbrain raphe nucleus inhibits episodic LH release and the LH ovulatory surge in rats [1,2], The raphe inhibition is via a serotonergic mechanism [1]. Thus, although mammals apparently have some LH inhibitory mechanisms, they do not have a GRIF system similar to that described here for goldfish.…”

Comparative study of the sources of neuronal projections to the site of gonadotrophin-releasing hormone perikarya and to the anteroventral periventricular nucleus in female rats

“…Distinct reproductive roles for these nuclei are suggested by functional studies. Thus, electrochemical stimulation of the median raphe nucleus in rats on the afternoon of proestrus blocks ovulation (Barofsky, 1979;Morello and Taleisnik, 1985). This effect can also be produced by electrolytic lesioning of the dorsal, but not the median, raphe nucleus (Morello and Taleisnik, 1985); there is evidence that this blocking of ovulation may involve removal of a 5-hydroxytryptamine (5-HT) projection from the dorsal raphe nucleus to the locus coeruleus (Morello and Taleisnik, 1988).…”