A Comparison of the Effects of Medial Preoptic Electrical Versus Electrochemical Stimulation on Luteinizing Hormone-Releasing Hormone Neuronal Responsiveness to Norepinephrine

Recently, we reported that luteinizing hormone‐releasing hormone (LHRH) neurons of estrogen‐treated, ovariectomized rats have only limited responsiveness to norepinephrine (NE). These conclusions were based upon observations that NE, when infused intracerebroventricularly, produced only minor increases in plasma luteinizing hormone (LH), whereas, similar infusions following preliminary medial preoptic area (MPOA) electrochemical stimulation (ECS) markedly amplified LH secretion. One difficulty with this approach is that ECS produces an irritative lesion and deposits iron within the tissue, whereas, electrical stimulation (ES) does not have such effects. Accordingly, in the present study, we compared the effects of MPOA–ECS versus –ES on LHRH neuronal responsiveness to NE. While equivalent peak LH concentrations occurred within 15 min after MPOA–ECS or –ES, in the ECS group, LH release was sustained, whereas, it abruptly ceased upon termination of ES (at 15 min). The intracerebroventricular pulse infusion of NE at the time of peak LH secretion (30 min) in MPOA–ECS animals markedly amplified LH release. In these animals, plasma LH remained significantly elevated for 75 min before a decline was observed. In contrast, an infusion of NE at the time of maximal LH release in ES rats (16 min) did not augment LH secretion. The second series of studies examined the effects of MPOA infusions of NE in animals receiving preoptic ES. A single infusion of NE 16 min after ES (i.e. one min after termination of ES) did not amplify LH release, but when two NE pulses were given at 5 and 16 min after beginning preoptic ES, peak plasma LH levels were maintained for an additional 30 min before a decline occurred. Pretreatment of rats with a yS‐adrenoreceptor antagonist (propranolol) or a monoamine oxidase inhibitor did not affect peak LH responses obtained after either MPOA–ES alone or combined with two pulses of NE infused into the MPOA at 5 and 16 min. We conclude that following cessation of MPOA–ES, LHRH neurons rapidly lose their responsiveness to NE, whereas, rats which received MPOA–ECS retain such responsiveness possibly due to the stimulative properties of the iron deposited by the ECS. Presumably, for NE to trigger an LH surge requires prior removal of some intrinsic inhibitory control which regulates LHRH neuronal responsiveness to NE.