Oestrogen Modulation of Excitatory Al Noradrenergic Input to Rat Medial Preoptic Gamma Aminobutyric Acid Neurones Demonstrated by Microdialysis

Herbison, Allan E.; Heavens, R.P.; Dyer, R. G.

doi:10.1159/000125568

Cited by 70 publications

(37 citation statements)

References 17 publications

(26 reference statements)

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“…Specifically, stimulation of the A l cell group in the brainstem of the rat during oestradiol negative feedback induces an immediate release of N A and GABA in the POA. This electrically-evoked release of GABA is blocked by an cr-adrenergic antagonist (42). However, when an identical experiment was performed in the preovulatory period, stimulation induced N A but not GABA release.…”

Section: Poamentioning

confidence: 88%

“…These data are in general agreement with those demonstrating that the turnover of N A increases prior to or during the surge (10,41) and that mean NA release in the POA is augmented immediately prior to the surge (IS). Recent studies have demonstrated that the actions of N A in the POA are mediated by GABA neurons (19,42). Specifically, stimulation of the A l cell group in the brainstem of the rat during oestradiol negative feedback induces an immediate release of N A and GABA in the POA.…”

Section: Poamentioning

confidence: 99%

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Changes in the Release of Gamma‐Aminobutyric Acid and Catecholamines in the Preoptic/Septal Area Prior to and During the Preovulatory Surge of Luteinizing Hormone in the Ewe

Robinson

Kendrick

Lambart

1991

J Neuroendocrinology

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The technique of intracranial microdialysis was used to monitor changes in the outflow of the catecholamines, noradrenaline, adrenaline and dopamine and the inhibitory amino-acid y-arninobutyric acid (GABA) in the preopticlseptal area of the conscious ewe during an oestradiol-induced surge of luteinizing hormone (LH). The s a m e animals were sampled twice from an identical brain site, once in the presence of oestradiol and once in its absence, when no surge occurred and LH levels remained low. Changes in the outflow of GABA, noradrenaline and adrenaline (but not dopamine) were related to changes in LH secretion. Specifically, GABA outflow was maximal in the h o u r s following oestradiol administration but began a sustained fall some 10 h before the surge began, to level off just before the first increment in LH secretion. Low GABA concentrations were maintained until after gonadotrophin levels had once more returned to baseline. The release of all three catecholamines was pulsatile. Noradrenergic activity was greater in the presence of oestradiol although activity did not alter over t h e 20 h of sampling. The pulse frequency of adrenaline was maximal in the h o u r s immediately prior to the LH surge and minimal in the hours following its initiation. These data suggest that a decrease in GABAergic transmission in t h e vicinity of t h e LH-releasing hormone cell bodies is a necessary component of the neural mechanism by which the oestradiol-induced surge of LH is generated. A general increase in noradrenergic activity coupled with changes in the release of adrenaline at t h e time of the surge may be additional prerequisites for successful ovulation.The hormonal events which are required to elicit the massive increment in luteinizing hormone (LH) secretion necessary to cause ovulation are relatively well understood and allow us, to some degree, to manipulate both our own fertility and that of other species ( I , 2). In contrast, the neural events which are a prerequisite for the LH surge remain largely enigmatic.Our knowledge has recently been extended by data demonstrating conclusively that the oestradiol-induced LH surge in the ewe results from a massive increase in the secretion of LH-releasing hormone (LHRH) into the portal vessels from nerve terminals located in the median eminence (3, 4). The cell bodies of these LHRH neurons are located in the preoptic and septa1 areas (POA/S) of the ovine brain ( 5 ) but as these cells d o not themselves possess oestrogen receptors (6), other steroid-sensitive neural elements must mediate oestrogen effects on LH. In relation to this, the POA is innervated by neurons containing the catecholamine neurotransmitters noradrenaline (NA; 7, 8) adrenaline (A; 9) and dopamine (DA; 10) and the inhibitory amino-acid y-aminobutyric acid (GABA; 1 I , 12). NA and GABA neurons have been shown to concentrate oestrogen (1 3-1 5 ) and all four neuroactive substances have been implicated in mediating the actions of gonadal steroids on LH secretion (16,17). This study sought to d...

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Section: Poamentioning

confidence: 88%

Section: Poamentioning

confidence: 99%

Changes in the Release of Gamma‐Aminobutyric Acid and Catecholamines in the Preoptic/Septal Area Prior to and During the Preovulatory Surge of Luteinizing Hormone in the Ewe

Robinson

Kendrick

Lambart

1991

J Neuroendocrinology

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“…It should be noted, however, that the stimulatory influence of NE within the GnRH network is mediated by ␣ 1 -adrenergic receptors (61, 315, 316, 329). Evidence for the indirect regulation of GnRH neurons by NE also exists and may involve, at least, a serial arrangement between NE, GABA, and GnRH neurons in the rat (264,326,330). The location and exact targets of NE neurons that may influence GnRH secretion at the level of the nerve terminals within the median eminence are unknown (331).…”

Section: Neurotensinmentioning

confidence: 99%

Multimodal Influence of Estrogen upon Gonadotropin-Releasing Hormone Neurons

1998

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“…Microdialysis studies have demonstrated that electrical stimulation of A1 noradrenergic groups stimulates the release of norepinephrine in the MnPO (49,59 of MnPO neurons that project to the PVN. This excitatory response was blocked by the α-adrenoceptor antagonist phentolamine, but not by the β-adrenoceptor antagonist timolol.…”

Section: The Anteroventral Third Ventricle Regionmentioning

confidence: 99%

Involvement of catecholaminergic medullary pathways in cardiovascular responses to acute changes in circulating volume

Cravo

Lopes

Pedrino

2011

Braz J Med Biol Res

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Water deprivation and hypernatremia are major challenges for water and sodium homeostasis. Cellular integrity requires maintenance of water and sodium concentration within narrow limits. This regulation is obtained through engagement of multiple mechanisms and neural pathways that regulate the volume and composition of the extracellular fluid. The purpose of this short review is to summarize the literature on central neural mechanisms underlying cardiovascular, hormonal and autonomic responses to circulating volume changes, and some of the findings obtained in the last 12 years by our laboratory. We review data on neural pathways that start with afferents in the carotid body that project to medullary relays in the nucleus tractus solitarii and caudal ventrolateral medulla, which in turn project to the median preoptic nucleus in the forebrain. We also review data suggesting that noradrenergic A1 cells in the caudal ventrolateral medulla represent an essential link in neural pathways controlling extracellular fluid volume and renal sodium excretion. Finally, recent data from our laboratory suggest that these structures may also be involved in the beneficial effects of intravenous infusion of hypertonic saline on recovery from hemorrhagic shock.

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Oestrogen Modulation of Excitatory Al Noradrenergic Input to Rat Medial Preoptic Gamma Aminobutyric Acid Neurones Demonstrated by Microdialysis

Cited by 70 publications

References 17 publications

Changes in the Release of Gamma‐Aminobutyric Acid and Catecholamines in the Preoptic/Septal Area Prior to and During the Preovulatory Surge of Luteinizing Hormone in the Ewe

Changes in the Release of Gamma‐Aminobutyric Acid and Catecholamines in the Preoptic/Septal Area Prior to and During the Preovulatory Surge of Luteinizing Hormone in the Ewe

Multimodal Influence of Estrogen upon Gonadotropin-Releasing Hormone Neurons

Involvement of catecholaminergic medullary pathways in cardiovascular responses to acute changes in circulating volume

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