Comparison of the effect of electrochemical stimulation of the medial preoptic area and the hypothalamic arcuate nucleus upon LH release in ovariectomized and proestrous rats.

Kawakami, Michiyuki; Higuchi, Takashi

doi:10.1507/endocrj1954.27.239

Cited by 3 publications

(2 citation statements)

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“…It is not clear in rats whether the rhythm origi nates from the medial basal hypothalamus or not, but the ARC contains high levels of LH-RH [6] and electrochemi cal stimulation of the ARC induces a rapid increase in se rum LH, though MPO stimulation fails to facilitate LH re lease in ovariectomized rats [10]. The findings of Séiâlô et al [15] revealed that no LH-RH positive cell bodies could be seen in the ARC though numerous LH-RH positive fi bers passed through the ARC in rats.…”

Section: Discussionmentioning

confidence: 99%

Electrophysiological Correlates of Pulsatile Gonadotropin Release in Rats

1982

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In order to reveal the electrophysiological correlates of pulsatile LH release in ovariectomized rats, changes in multiple unit activity (MUA) in the arcuate nucleus (ARC), the medial preoptic area, the ventromedial nucleus, the anterior hypothalamic area and other areas of the brain were recorded in lightly anesthetized female rats. Rats were ovariectomized at least 7 weeks prior to the experiment. 0.1-ml blood samples were withdrawn from a cardiac catheter at 10-min intervals during the recording in order to measure the changes in the plasma LH concentration by radioimmunoassay. The LH concentration showed pulsatile changes under continuous intravenous infusion of thiopental sodium while cortical EEG was stable throughout the experiment. The firing rate in the middle part of the ARC (8 recordings) changed in parallel with the increase in the plasma LH concentration and was abruptly raised just prior to an increase in LH secretion. The number of MUA spike discharges per minute increased to 1.5–5 times that of the basal level. MUA started to increase 2–9 min prior to the LH rise and the high level of MUA lasted for 1–5 min. The firing rate in the ARC (14 recordings) and in other areas (54 recordings) recorded did not change periodically in parallel with the increase in LH. As these changes in MUA were localized in the ARC and were not reflected in cortical EEG, they might be specific local changes distinguished from generalized systemic effects involving the whole brain. These extreme increases in MUA seem to be due to the high activity either of neurons that secrete LH-RH or those that control the secretion of LH-RH.

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Section: Discussionmentioning

confidence: 99%

Electrophysiological Correlates of Pulsatile Gonadotropin Release in Rats

1982

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“…The increased amplitude of a single LH pulse was observed in intact rats following longer immobili zation stress [unpubl. observations], electrical stimulation of the brain in rats [15], or after the suppression of LH re lease by estrogen or neurotransmitter blockers in ovariec tomized monkeys [3,37]. Increased amplitude and duration of LH pulses following the period of inhibition appeared in intact animals, but in the rats lacking some component which regulate the pulsatile release of anterior pituitary hor mone as the animals with a small anterior cut, might exhibit greater pulses of hormone release without inhibitory period.…”

Section: Discussionmentioning

confidence: 99%

Effect of Partial Deafferentation of the Hypothalamus on Stress-Induced LH Suppression and Prolactin Release

Kawakami

Higuchi

1981

Neuroendocrinology

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Stress of immobilization suppressed pulsatile LH release and decreased mean serum LH levels within 10 min, lasting at least for 2 h in ovariectomized rats. Anterior cuts (radius, 2 mm) at the level of the caudal border of the suprachi-asmatic nucleus, resulted in elimination of the stress-induced LH suppression. A smaller cut (radius, 1 mm) at the same level induced increased LH secretion without a period of inhibition in some rats by the stress. Extended anterior cut at the level of the border between the medial preoptic and the anterior hypothalamic area, partially inhibited the suppressive effect of the stress on LH secretion; that is, LH pulses resumed within 2 h. A more extended anterior cut at the level of the anterior border of the medial preoptic area, or a posterior or small posterior cut at the level of the midmammillary body, had no effect on the LH suppression by the stress. Basal LH levels prior to the stress were lower in the groups which had neural deafferentation in the anterior area to the mediobasal hypothalamic, but not in the groups with posterior deafferentation, compared with the sham control. Serum prolactin response to the immobilization was inhibited almost completely by an anterior, small anterior, posterior or small posterior cut. Extended anterior cuts inhibited the stress-induced prolactin release in about half of the animals, whereas a more extended anterior cut had no effect. Any kind of deafferentation except the posterior or small posterior cut failed to change basal nonstressed prolactin levels as compared to those in sham-operated rats. The rats bearing a posterior or small posterior cut had significantly lower serum prolactin levels prior to the immobilization. These results indicate that the stimulus necessary for stress-induced LH suppression and for the maintenance of the basal LH levels may reach the mediobasal hypothalamus from the anterior direction. The stress-evoked inhibitory stimulus for LH-RH release may interact, at the anterior hypothalamus-suprachiasmatic region, with the LH-RH neuron or inputs regulating the LH-RH neuron. Both neural connections from anterior and posterior directions to the medial basal hypothalamus seem to be indispensable for the stress-induced prolactin release and the input from the posterior direction for maintaining the nonstressed basal prolactin levels.

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Unifying effectors of circadian rhythm: Protein N -acetylation, phosphorylation, sulfation and other electrical effects

Kovacic¹,

Somanathan²

2014

Journal of Electrostatics

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Comparison of the effect of electrochemical stimulation of the medial preoptic area and the hypothalamic arcuate nucleus upon LH release in ovariectomized and proestrous rats.

Cited by 3 publications

References 15 publications

Electrophysiological Correlates of Pulsatile Gonadotropin Release in Rats

Electrophysiological Correlates of Pulsatile Gonadotropin Release in Rats

Effect of Partial Deafferentation of the Hypothalamus on Stress-Induced LH Suppression and Prolactin Release

Unifying effectors of circadian rhythm: Protein N -acetylation, phosphorylation, sulfation and other electrical effects

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