Electrophysiological analysis of inhibitory synaptic mechanisms in the preoptic area of the rat.

Mayer, Mark L.

doi:10.1113/jphysiol.1981.sp013791

Cited by 18 publications

(6 citation statements)

References 41 publications

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“…GABA-dependent whole-cell currents were evident in 9l% of VMN neurons tested from females and 90% of VMN neurons from males of all ages, consistent with pre vious reports of GABA sensitivity for neurons in other hypothalamic nuclei in the rat [48,49] and were reversi bly blocked by bicuculline (3 of 3 neurons tested). In agreement with previous studies in cortical [50] and pitu itary neurons [51], GABA responses elicited during these brief recording periods, usually no more than a few min utes after seal formation, did not demonstrate rundown of the peak current amplitude [52], and inclusion of 2 mM ATP in the pipette solution did not affect the properties of responses.…”

Section: Resultssupporting

confidence: 67%

GABA<sub>A</sub> Receptor-Mediated Responses in the Ventromedial Nucleus of the Hypothalamus of Female and Male Neonatal Rats

Smith¹,

Brennan

Clark

et al. 1996

Neuroendocrinology

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Perinatal exposure of the developing brain to gonadal steroids during a limited critical period induces permanent, organizational differences in neural structures between male and female animals. These differences are believed to underlie the manifestation of sexually dimorphic behaviors. Gamma-amino-butyric acid type A (GABAA) receptors expressed in the ventromedial nucleus (VMN) of the hypothalamus appear to be a key component underlying the expression of sexually dimorphic behaviors in rats. Specifically, GABA_Areceptor levels are known to be steroid regulated and sexually dimorphic, and GABAA-mediated transmission within the VMN is critical for the expression of sexual behavior in female, but not male, rats. Here we report that analysis of VMN neurons from neonatal rats revealed significant sex-specific differences in GABA_A receptor channel properties. Specifically, GABA_A-mediated currents elicited by direct agonist application decayed more rapidly in VMN neurons from females than from males. Kinetic differences became more pronounced during the first 2 weeks of postnatal development. Analysis of small, spontaneous inhibitory postsynaptic currents recorded in intact slices indicated a trend towards slower responses in neurons from males than females, but the differences in decay kinetics were not significant. Sex-specific differences in GABAA receptor kinetics may arise from activation of receptors not receiving synaptic contacts in the slice preparation or may become apparent at intact synapses under conditions of increased activity and evoked release.

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Section: Resultssupporting

confidence: 67%

GABA<sub>A</sub> Receptor-Mediated Responses in the Ventromedial Nucleus of the Hypothalamus of Female and Male Neonatal Rats

Smith¹,

Brennan

Clark

et al. 1996

Neuroendocrinology

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“…If this is the case, the c&y, isoform of the GABA, receptor, which may also exist in the medial amygdala (see Wisden et al, 1992), would provide a selective pharmacological target for limbic and neuroendocrine networks in the brain. To our knowledge, the pharmacology of an expressed o,&y, GABA, receptor isoform has not been examined, although extracellular recordings in vivo have shown inhibitory responses from almost all cells in the POA in response to GABA (Mayer, 1981).…”

Section: Discussionmentioning

confidence: 99%

Estrogen regulation of GABAA receptor subunit mRNA expression in preoptic area and bed nucleus of the stria terminalis of female rat brain

1995

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This study has examined whether circulating estrogens are involved in regulating y-aminobutyric acid (GABA), receptor mRNA expression in regions of the female rat brain known to contain estrogen receptors (ERs). In situ hybridization experiments using 35S-labeled oligonucleotides specific for %, B3, and y, subunit mRNAs of the GABA, receptor demonstrated that all three mRNAs were abundant in only the medial preoptic nucleus (MPN), where they were expressed by the vast majority of cells, and specific regions of the bed nucleus of the stria terminalis including the principle encapsulated nucleus (PrN-BNST) and bed nucleus of the anterior commissure (BNAC). Estrogen treatment of ovariectomized rats for 7 d resulted in significant 30-60% increases in QL~ and Y,, but not p3, subunit mRNA expression in the MPN and PrN-BNST. Estrogen treatment for 24 hr resulted in levels of mRNA expression intermediate between those of controls and animals treated with estrogen for 7 d. No changes in subunit mRNA expression were detected for any subunit in the BNAC or cingulate cortex. Double-labeling immunocytochemistry experiments using antibodies directed against the cll, subunit of the GABA, receptor and the ER, revealed that 67 f 3% of % subunit-immunoreactive cells in the MPN also contained ER immunoreactivity. Cells expressing OL* subunits in the PrN-BNST were also found to possess ERs while those in the BNAC and cingulate cortex did not. These findings suggest the possibility that ER-containing cells in the MPN and PrN-BNST express an c&-y, isoform of the GABA, receptor that has its (II, and y, subunits regulated by circulating estrogen concentrations. Together, our observations indicate that estrogen may regulate GABA,, receptor mRNA expression at a transcriptional level and that this is only likely to occur within regions of the rat brain possessing ERs.

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“…Few GABAb receptors are found in the hypothalamus [18], and, in the MPOA, approximately 90% of the inhibitory effects of GABA on neurones can be blocked by bicuculline [19]. Furthermore, baclofen, the GABAb receptor agonist, does not alter LHRH secretion from the hypothalamic slice preparation [20], Immediately prior to and during the LH surge, we have surprisingly found no evidence for a tonic action of GABA, act ing through the post-synaptic GABA..\ receptor, on neural ele ments in the MPOA regulating the LH surge.…”

Section: Discussionmentioning

confidence: 99%

Effect on Luteinizing Hormone Secretion of GABA Receptor Modulation in the Medial Preoptic Area at the Time of Proestrous Luteinizing Hormone Surge

Herbison

Dyer²

1991

Neuroendocrinology

130

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Using a bilateral medial preoptic area (MPOA) infusion system in conscious female rats we have investigated the role of the GABA system in this area on the proestrous luteinizing hormone (LH) surge. Fifteen-minute blood samples for LH estimation were taken throughout the afternoon of proestrus from female rats exhibiting 4-day oestrous cycles and implanted at least 2 weeks prior with cerebral guide cannulae. Between 15:00 and 17:00 h rats received an infusion (1 µl/30 min) of artificial cerebro-spinal fluid (n = 7), 10 µM GABA (n = 6) or 10 µM bicuculline methiodide (BMI, n = 6). Animals infused with GABA failed to exhibit an LH surge, while BMI-treated animals displayed an LH surge which was not significantly different to controls. These data show that on the afternoon of proestrus, there are no tonic modulatory actions of the GABA system, acting through the GABAA receptor, on neural elements controlling the LH surge in the MPOA. If however, GABA levels are elevated in the MPOA at this time then the LH surge is blocked. In conjunction with data from correlative studies showing a decrease in endogenous GABA release prior to the LH surge, we suggest that this fall in activity is an essential component of the LH surge mechanism.

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Electrophysiological analysis of inhibitory synaptic mechanisms in the preoptic area of the rat.

Cited by 18 publications

References 41 publications

GABA<sub>A</sub> Receptor-Mediated Responses in the Ventromedial Nucleus of the Hypothalamus of Female and Male Neonatal Rats

GABA<sub>A</sub> Receptor-Mediated Responses in the Ventromedial Nucleus of the Hypothalamus of Female and Male Neonatal Rats

Estrogen regulation of GABAA receptor subunit mRNA expression in preoptic area and bed nucleus of the stria terminalis of female rat brain

Effect on Luteinizing Hormone Secretion of GABA Receptor Modulation in the Medial Preoptic Area at the Time of Proestrous Luteinizing Hormone Surge

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