Differential Effects of GABA&lt;sub&gt;A&lt;/sub&gt; and GABA&lt;sub&gt;B&lt;/sub&gt; Receptor Agonists on NMDA-Induced and Noradrenaline Induced Luteinizing-Hormone Release in the Ovariectomized Estrogen-Primed Rat

Akema, Tatsuo; Kimura, Fukuko

doi:10.1159/000126338

Cited by 29 publications

(15 citation statements)

References 25 publications

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“…Stryker et al [13]have postulated that GABA and GABAergic drugs, like baclofen, may modulate somatostatin secretion via the calcium-dependent GABA B receptors, and the basal GH release acting on hypothalamus [14]. On the other hand, a peripheral action of baclofen at pituitary level is not possible since this drug does not affect GH release from the rat pituitary gland in vitro [4].…”

Section: Discussionmentioning

confidence: 99%

Growth Hormone Secretion after Baclofen Administration in Different Phases of the Menstrual Cycle in Healthy Women

Orio

Palomba²,

Colao

et al. 2001

Horm Res Paediatr

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Aim: The aim of this study was to investigate the effect of baclofen administration on growth hormone (GH) secretion during different phases of the menstrual cycle. Methods: Twelve healthy women (33.6 ± (SD) 2.8 years; range 23–40 years) with regular menstrual cycles were enrolled. The phases of the menstrual cycle were determined using transvaginal ultrasonography (TV-US) and detecting hormonal serum levels. Plasma GH levels were evaluated during the early follicular, periovulatory and luteal phases of the cycle before and after the baclofen challenge test. Results: After acute baclofen administration, GH levels increased significantly (p < 0.001) compared to basal values during the periovulatory and luteal phases, while no significant variation was detected during the early follicular phase. In addition, plasma GH levels resulted significantly (p < 0.001) higher during the luteal phase than during the periovulatory phase. Conclusion: Acute baclofen administration induces a significant increase in plasma GH levels in healthy females during the periovulatory and luteal phases, but not during the early follicular phase. These data suggest a modulator role of plasma sex steroids levels on GH release induced by baclofen.

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Section: Discussionmentioning

confidence: 99%

Growth Hormone Secretion after Baclofen Administration in Different Phases of the Menstrual Cycle in Healthy Women

Orio

Palomba²,

Colao

et al. 2001

Horm Res Paediatr

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“…3, 32, 33]. With respect to NMDA recep tors, there is an abundance of evidence showing that NMDA stimulates GnRH and LH release [4][5][6][7][8][9][10][11][12], induces AMPA Receptors and GnRH Secretion pulsatile LH release [22,34,35] and that NMDA recep tors mediate, at least in part, steroid signals in the hypo thalamus to produce the steroid-induced and preovulato ry LH surge in the female [12][13][14][15]19], Kainate-type gluta mate receptors have also received attention, and activa tion of these receptors has been shown to enhance GnRH and LH release in female animals [6,34]; however, kai nate receptors have been demonstrated to desensitize rap idly with respect to stimulation of LH secretion, casting doubt on whether these receptors play an important role in LH surge expression in females [34,35].…”

Section: Discussionmentioning

confidence: 99%

“…1 for review and ref. 3,4,[7][8][9][10][11][12][13], and a role has been suggested for glutamate in the produc tion of the steroid-induced and preovulatory LH surge in the female rat [4,[14][15][16].…”

Section: Introductionmentioning

confidence: 99%

“…Due to early availability of agonists and antagonists for the N-methyl-D-aspartate (NMDA) type of the glutamate receptor, work has been completed which suggests that NMDA receptors mediate, at least in part, glutamate effects on GnRH and LH release in female animals. For instance, NMDA receptors have been demonstrated to be localized in key female hypothalamic nuclei responsible for regulat ing GnRH secretion [17], NMDA treatment has been shown to stimulate GnRH and LH release in female ani mals [4][5][6][7][8][9][10][11][12][13]17] and administration of specific NMDA receptor antagonists has been demonstrated to signifi cantly attenuate the steroid-induced and preovulatory LH surge in female rats [4. 8, 14-19], The mechanism where by activation of NMDA receptors leads to enhanced GnRH secretion is not fully understood, but NMDA receptors have been demonstrated to be colocalized in nit ric oxide (NO) neurons in the female rat hypothalamus [17], suggesting that NO may act as a mediator of glutamate/NMDA effects in the hypothalamus.…”

Section: Introductionmentioning

confidence: 99%

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Regulation of Gonadotropin-Releasing Hormone and Luteinizing Hormone Secretion by AMPA Receptors

et al. 1997

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Recent work has demonstrated that glutamate functions as a major transmitter involved in the regulation of gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH) secretion in female animals, although the specific receptors and mechanisms mediating its effects have not been completely worked out. The purpose of the present study, therefore, was to examine the role of the AMPA (α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid)-type glutamate receptor in the control of GnRH and LH secretion in female animals. Toward this end, the dose- and steroid-dependent effects of AMPA on GnRH and LH secretion in female rats were investigated using both in vitro and in vivo approaches, and the role of AMPA receptors in the production of the steroid-induced LH surge was also assessed. The results of the study revealed that central administration of AMPA resulted in a stimulation of LH release in the estrogen-primed ovariectomized adult rat. AMPA was also found to potently stimulate GnRH release in vitro from mediobasal hypothalamic (MBH) fragments obtained from estrogen-primed ovariectomized adult rats, and this effect was blocked by the selective AMPA receptor antagonist, NBQX. The mechanism of action of AMPA appeared to differ from that of N-methyl-D-aspartate (NMDA) as AMPA, in contrast to NMDA, failed to elevate nitric oxide synthase activity in the hypothalamus. The effect of AMPA on LH secretion was demonstrated to be steroid dependent, as central administration of AMPA stimulated LH release in estrogen-primed ovariectomized rats, but was inhibitory to LH release in non-estrogen-primed ovariectomized rats. In contrast, AMPA stimulated GnRH release equally well from MBH fragments obtained from estrogen-primed or non-estrogen-primed ovariectomized rats. The different effects of AMPA on LH release may be due to different pituitary sensitivities between the two models, or alternatively, AMPA may stimulate the release of LH inhibitory factors in the ovariectomized rat in the absence of estrogen. Finally, a physiological role for AMPA receptors in the production of the steroid-induced LH surge was suggested, based on the finding that central administration of the selective AMPA receptor antagonist, NBQX, into the third cerebroventricle significantly attenuated the steroid-induced LH surge in the ovariectomized adult female rat.

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“…Control animals received the same volume o f the vehicle. The selected doses o f N M D A and AP5 were based on a pre vious dose-response study in our laboratory [ 13]. Doses o f C R H and [5-endorphin were comparable to those which had been shown to sup press the existing pulsatile L H secretion in ovariectomized rats [ l -4 , 14).…”

Section: Methodsmentioning

confidence: 99%

Differential Inhibition of NMDA- and Naloxone-lnduced LH Release by NMDA Receptor Antagonist and CRH in Ovariectomized Estrogen-Primed Rats

Chiba

Akema²,

Nagami³

et al. 1997

Neuroendocrinology

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A possible functional relationship between endogenous opioid peptides (EOPs), corticotropin-releasing hormone (CRH) and excitatory amino acids (EAAs) in the control of LH secretion was investigated in ovariectomized estrogen-primed rats. An intraventricular (icv) injection of an EAA agonist, N-methyl-D-aspartate (NMDA), or an EOP antagonist, naloxone, produced an abrupt increase in the serum LH level. While icv pretreatment of the animals with 2-amino-5-phosphonovaleric acid, a specific NMDA receptor antagonist, did not affect by itself basal LH levels, it significantly suppressed the NMDA-induced and also the naloxone-induced LH release. An icv injection of CRH also interfered with the naloxone-induced LH release. However, the NMDA-induced LH release was not affected by an icv injection of CRH or of β-endorphin. These results suggest that the sites of EOP and CRH inhibition may be located upstream of the site of NMDA stimulation on the GnRH neuronal pathway, and that CRH can inhibit LH secretion without mediation by EOP neurons.

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Differential Effects of GABA<sub>A</sub> and GABA<sub>B</sub> Receptor Agonists on NMDA-Induced and Noradrenaline Induced Luteinizing-Hormone Release in the Ovariectomized Estrogen-Primed Rat

Cited by 29 publications

References 25 publications

Growth Hormone Secretion after Baclofen Administration in Different Phases of the Menstrual Cycle in Healthy Women

Growth Hormone Secretion after Baclofen Administration in Different Phases of the Menstrual Cycle in Healthy Women

Regulation of Gonadotropin-Releasing Hormone and Luteinizing Hormone Secretion by AMPA Receptors

Differential Inhibition of NMDA- and Naloxone-lnduced LH Release by NMDA Receptor Antagonist and CRH in Ovariectomized Estrogen-Primed Rats

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