In vivo GABA release from the medial preoptic area of diestrous and ovariectomized rats

1982 ◽  
Vol 46 (1) ◽  
pp. 69-72 ◽  
Author(s):  
J. Ondo ◽  
T. Mansky ◽  
W. Wuttke
Keyword(s):  
Preoptic Area ◽  
Gaba Release ◽  
Medial Preoptic Area ◽  
Ovariectomized Rats

scholarly journals The Excitatory Peptide Kisspeptin Restores the Luteinizing Hormone Surge and Modulates Amino Acid Neurotransmission in the Medial Preoptic Area of Middle-Aged Rats

Endocrinology ◽  
2009 ◽  
Vol 150 (8) ◽  
pp. 3699-3708 ◽  
Author(s):  
Genevieve Neal-Perry ◽  
Diane Lebesgue ◽  
Matthew Lederman ◽  
Jun Shu ◽  
Gail D. Zeevalk ◽  
...  
Keyword(s):  
Positive Feedback ◽  
Preoptic Area ◽  
Gaba Release ◽  
Medial Preoptic Area ◽  
Aged Rats ◽  
Middle Aged ◽  
Lh Surge ◽  
Age Related ◽  
Lh Release ◽  
Estrogen Positive Feedback

Reproductive success depends on a robust and appropriately timed preovulatory LH surge. The LH surge, in turn, requires ovarian steroid modulation of GnRH neuron activation by the neuropeptide kisspeptin and glutamate and γ-aminobutyric acid (GABA) neurotransmission in the medial preoptic area (mPOA). Middle-aged females exhibit reduced excitation of GnRH neurons and attenuated LH surges under estrogen-positive feedback conditions, in part, due to increased GABA and decreased glutamate neurotransmission in the mPOA. This study tested the hypothesis that altered kisspeptin regulation by ovarian steroids plays a role in age-related LH surge dysfunction. We demonstrate that middle-aged rats exhibiting delayed and attenuated LH surges have reduced levels of Kiss1 mRNA in the anterior hypothalamus under estrogen-positive feedback conditions. Kisspeptin application directly into the mPOA rescues total LH release and the LH surge amplitude in middle-aged rats and increases glutamate and decreases GABA release to levels seen in the mPOA of young females. Moreover, the N-methyl-d-aspartate receptor antagonist MK801 blocks kisspeptin reinstatement of the LH surge. These observations suggest that age-related LH surge dysfunction results, in part, from reduced kisspeptin drive under estrogen-positive feedback conditions and that kisspeptin regulates GnRH/LH release, in part, through modulation of mPOA glutamate and GABA release.

Further evidence that preoptic anterior hypothalamic GABAergic neurons are part of the GnRH pulse and surge generator

1988 ◽  
Vol 118 (4) ◽  
pp. 573-579 ◽  
Author(s):  
Hubertus Jarry ◽  
Astrid Perschl ◽  
Wolfgang Wuttke
Keyword(s):  
Corn Oil ◽  
Gaba Release ◽  
Gabaergic Neurons ◽  
Ovariectomized Rats ◽  
Release Rates ◽  
Hypothalamic Area ◽  
Lh Surge ◽  
Lh Release ◽  
Previous Demonstration

Abstract. The in vivo release rates of GABA from the preoptic/anterior hypothalamic area (PO/AH) of ovariectomized rats were assessed by means of a focal perfusion cannula system. Seven days after surgery all animals received a sc silastic capsule implant containing either estradiol-17β (E2) or corn oil, and they were perfused 3 days later. Perfusate fractions were sampled at 5-min intervals and blood was collected every 10 min over a period of 5 h. In ovariectomized animals PO/AH GABA release was pulsatile without any diurnal rhythm. Prior to frequence analysis by means of the pulsar-programme, LH and GABA values were z-transformed. Significant LH peaks of all examined ovariectomized rats were superimposed and GABA data were arranged accordingly. It became evident that LH episodes are preceded by a significant reduction of preoptic anterior hypothalamic GABA release. The secretion patterns of GABA and LH were profoundly affected by E2 replacement. During early noon when LH levels were low, constantly elevated hypothalamic GABA release rates were observed in E2-substituted rats in comparison to ovariectomized rats. GABA release rates fell significantly during the E2-induced LH surge. Our previous demonstration of the existence of a large number of estrogen-respective GABAergic neurons in the PO/AH is suggestive of these neurons changing their activity in response to estrogen treatment. We conclude that these estrogen-respective GABAergic neurons are involved in the generation of GnRH pulses as well as in the generation of the so-called positive feedback effect of E2 on LH release. Whether the same GABAergic neurons have those effects or whether two populations of GABAergic neurons exist, one responsive for generation of pulsatile LH release, the other responsive for the estrogen-induced LH surge, remains to be elucidated.

Oestrogen and noradrenaline modulate endogenous GABA release from slices of the rat medial preoptic area

1989 ◽  
Vol 486 (1) ◽  
pp. 195-200 ◽  
Author(s):  
Allan E. Herbison ◽  
Robert P. Heavens ◽  
Richard G. Dyer
Keyword(s):  
Preoptic Area ◽  
Gaba Release ◽  
Medial Preoptic Area ◽  
Endogenous Gaba

GABA release in the medial preoptic area of cyclic female rats

Neuroscience ◽  
2002 ◽  
Vol 113 (1) ◽  
pp. 109-114 ◽  
Author(s):  
D Mitsushima ◽  
T.-T.-W Shwe ◽  
T Funabashi ◽  
K Shinohara ◽  
F Kimura
Keyword(s):  
Preoptic Area ◽  
Gaba Release ◽  
Medial Preoptic Area ◽  
Female Rats

Varying sensitivity to the negative oestrogen feedback during the ovarian cycle of female rats: evidence for the involvement of oestrogen and the medial preoptic area

1984 ◽  
Vol 102 (3) ◽  
pp. 287-294 ◽  
Author(s):  
F. Döcke ◽  
W. Rohde ◽  
P. Gerber ◽  
R. Chaoui ◽  
G. Dörner
Keyword(s):  
Preoptic Area ◽  
Medial Preoptic Area ◽  
Ovarian Cycle ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Adult Rats ◽  
Gonadotrophin Secretion ◽  
Arcuate Region ◽  
Lh Secretion ◽  
Follicle Maturation

ABSTRACT The gonadotrophic response to a single injection of oestradiol benzoate (OB) was studied in acutely ovariectomized adult rats during the different stages of a 4-day ovarian cycle. The results showed a sudden decline of the sensitivity to the gonadotrophin-inhibiting effect of OB between metoestrus and dioestrus. This desensitization to the negative oestrogen feedback was probably caused by an oestrogen action on the medial preoptic area (MPOA). In rats ovariectomized and implanted with OB in the MPOA in metoestrus, an s.c. injection of OB on the presumptive day of pro-oestrus did not lower the circulating LH and FSH levels, whereas a clear suppression of gonadotrophin secretion was seen in females implanted with cholesterol in the MPOA or implanted with OB in the hypothalamic ventromedial–arcuate region. Similar findings were obtained in rats which had been ovariectomized 3–4 weeks before implantation. A final experiment demonstrated that bilateral lesioning of the MPOA also reduced the sensitivity to the negative feedback action of oestrogen in long-term ovariectomized rats. In all experiments performed, diminution of the oestrogen-induced inhibition of LH secretion was more marked than that of suppression of FSH secretion. It is proposed that desensitization to the negative oestrogen feedback, probably resulting from an inhibitory oestrogen action on medial preoptic neurones, is a prerequisite for adequate gonadotrophic support of preovulatory follicle maturation in the presence of a continuously rising oestrogen concentration in the blood. J. Endocr. (1984) 102, 287–294

scholarly journals Allopregnanolone enhancement of GABAergic transmission in rat medial preoptic area neurons

2002 ◽  
Vol 283 (6) ◽  
pp. E1257-E1265 ◽  
Author(s):  
Soko Uchida ◽  
Eiichiro Noda ◽  
Yasuhiro Kakazu ◽  
Yoshihito Mizoguchi ◽  
Norio Akaike ◽  
...  
Keyword(s):  
Preoptic Area ◽  
Gaba Release ◽  
Medial Preoptic Area ◽  
Presynaptic Terminal ◽  
Presynaptic Terminals ◽  
Primary Metabolite ◽  
Functional Connection ◽  
Gabaergic Transmission ◽  
Sex Steroid Hormone ◽  
Dynamics And Control

γ-Aminobutyric acid (GABA)-mediated transmission in the medial preoptic area (MPOA) of the hypothalamus plays an important role in functions such as sex steroid hormone dynamics and control of body temperature. The action of allopregnanolone, the primary metabolite of progesterone, on GABAergic transmission was investigated by employing patch clamp whole cell recording on acutely dissociated rat MPOA neurons with the functional connection of presynaptic terminals. Allopregnanolone enhanced spontaneous GABA release on the MPOA neurons and induced prolonged decay of miniature GABAergic-inhibitory postsynaptic currents (mIPSCs). The facilitation of GABA release from the presynaptic terminals by allopregnanolone disappeared in Ca2+-free extracellular solution. The presynaptic action of this neurosteroid was also blocked by bumetanide, a blocker of cation-Cl− cotransporters, and by removal of extracellular Na+. The results suggest that allopregnanolone enhances GABAergic transmission at the MPOA neurons by pre- and postsynaptic mechanisms. The enhancement of GABA release by allopregnanolone might require a high Cl− concentration in the presynaptic terminal maintained by Na+-dependent, bumetanide-sensitive mechanisms (e.g., Na+-K+-Cl− cotransporter) and might be mediated by Ca2+ influx into presynaptic terminal.

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