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Estrogen membrane g-protein-coupled receptor 30 and anxiety

Estrogen membrane G-protein-coupled receptor 30 and anxiety

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中国神经科学学会第十届全国学术会议

作者： Zhen TIAN Ming-gao ZHAO Department of Pharmacology School of PharmacyThe Fourth Military Medical University

Objective g-protein-coupled receptor 30（gPR30）/g-protein-coupled estrogen receptor is a novel estrogen membrane receptor that localizes to the cell membrane and endoplasmic reticulum.gPR30 is widely distributed and has numerous physiological functions in the central nervous system.However,the role of gPR30in modulating the balance between excitatory and inhibitory transmissions in the BLA remains unknown.Methods Experiments were performed in the ovariectomized（OVX） mice.Western-blot was used to detect the protein expression.Brain slice recordings were performed on the slice-containing the basolateral amygdala（BLA）.Results gPR30 expression in the amygdala of OVX mice significantly increased after acute stress and was accompanied by anxiety-like behaviors.We found that gPR30 is highly expressed in the BLA.Additionally,gPR30 expression in the amygdala of OVX mice significantly increased after acute stress and was accompanied by anxiety-like behaviors.These effects,however,were reversed by local infusion of the gPR30 agonist（g1） in the BLA.protein assessments revealed that g1 attenuated the up-regulation of the g1uR1 subunit of the a-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid（AMPA） receptor and NR2A-containing N-methyl-D-aspartate receptors（NMDARs） in the BLA of OVX mice using an acute stress paradigm.In the same model,we found that the agonist also blocked the down-regulation of γ-aminobutyric acid A（gABAa） receptors and NR2B-containing NMDARs.Electrophysiological recording showed that the activation of gPR30 increased the inhibitory synaptic transmission in the BLA.Conclusion Overall,our results indicate that estradiol reduces anxiety-like behaviors induced by acute stress at least partially through gPR30 signaling,maintaining the balance between gABAergic and glutamatergic transmission in the BLA of OVX-stressed mice.

关键词： estrogen g-protein-coupled receptor 30 stress anxiety

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Downregulated gPR30 Expression in the Epileptogenic Foci of Female Patients with Focal Cortical Dysplasia Type Ⅱb and Tuberous Sclerosis Complex Is Correlated with 18F-FDg PET-CT Values

Downregulated GPR30 Expression in the Epileptogenic Foci of ...

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第十六届中国医师协会神经外科医师年会

作者： Zhongke Wang Kaixuan Huang Xiaolin Yang Kaifeng Shen Ling Yang Ruotong Ruan Xianjun Shi Miao Wang gang Zhu Meihua Yang Chunqing Zhang Shengqing Lv Hui Yang Xiaotang Fan Shiyong Liu Department of Neurosurgery Xinqiao HospitalArmy Medical University (Third Military Medical University) Department of Developmental Neuropsychology School of PsychologyArmy Medical University (Third Military Medical University) Department of Basic Medical College Army Medical University (Third Military Medical University)

Focal cortical dysplasia type Ⅱb(FCDⅡb) and tuberous sclerosis complex(TSC) are typical causes of developmental delay and refractory epilepsy.g-protein-coupled receptor 30(gPR30) is a specific estrogen receptor that is critical in neurodevelopment,neuroinflammation,and neuronal excitability,suggesting that it plays a potential role in the epilepsy of patients with FCDⅡb and TSC.Therefore,we investigated the role of gPR30 in patients with FCDⅡb and TSC.We found that the expression of gPR30 and its downstream protein kinase A(PKA) pathway were decreased and negatively correlated with seizure frequency in female patients with FCDⅡb and TSC,but not in male patients.gPR30 was widely distributed in neurons,astrocytes,and microglia,and its downregulation was especially notable in microglia.The gPR30 agonist g-1 increased the expression of PKA and p-PKA in cultured cortical neurons,and the gPR30 antagonist g-15 exhibited the opposite effects of g-1.The NF-κB signaling pathway was also activated in the specimens of female patients with FCDⅡb and TSC,and was regulated by g-1 and g-15 in cultured cortical neurons.We also found that gPR30 regulated cortical neuronal excitability by altering the frequency of spontaneous excitatory postsynaptic currents and the expression of NR2A/B.Further,the relationship between gPR30 and glycometabolism was evaluated by analyzing the correlations between gPR30 and F-FDg PET-CT values(standardized uptake values,SUVs).Positive correlations between gPR30 and SUVs were found in female patients,but not in male patients.Intriguingly,gPR30 expression and SUVs were significantly decreased in the epileptogenic tubers of female TSC patients,and ROC curves indicated that SUVs could predict the localization of epileptogenic tubers.Taken together,our results suggest a potential protective effect of gPR30 in the epileptogenesis of female patients with FCDⅡb and TSC.

关键词： g-protein-coupled receptor 30 Focal cortical dysplasia type Ⅱb Tuberous sclerosis complex Whole-cell patch-clamp 18F-FDg Positron emission tomography-computerized tomography Standardized uptake values

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Fast nongenomic neuroprotection mediated by gPR30-dependent depression of NR2B-containing NMDA receptors

Fast nongenomic neuroprotection mediated by GPR30-dependent ...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Nan ZHANg,Ming-gao ZHAO~* Department of Pharmacology,School of Pharmacy,Fourth Military Medical University,Xi''an 710032,China

＜正＞17-β-Estradiol（E2） is a steroid hormone involved in neuroprotection against excitotoxicity and other forms of brain injury.Through genomic and non- genomic mechanisms,E2 modulates neuronal excitability and rapidly increases signal transmission by regulating N-methyl-D-aspartate（NMDA） and non-NMDA receptors.The potential neuroprotective role of estradiol in chronic neurodegenerative disorders and acute brain ischemia following cardiac arrest and stroke is of great therapeutic interest.However,the mechanisms and identity of the receptors involved remain unclear,although it has been suggested that g-protein-coupled receptor 30（gPR30） is linked to protection against ischemic insults.In this study,rapid nongenomic neuroprotection by gPR30 stimulation was examined in culture cortical neurons.Both E2 and the gPR30 agonist gl attenuated the excitotoxicity induced by NMDA receptor stimulation.The acute neuroprotection induced by gPR30 stimulation was dependent on g-protein coupled signaling and ERK1/2 activation,but independent of gene transcription and protein synthesis.Knockdown of gPR30 by transfection with small interfering RNAs（siRNAs） significantly reduced E2-induced rapid neuro- protection.Patchclamp recordings revealed that the activation of gPR30 significantly depressed exogenous NMDA-elicited currents. Short-term activation of gPR30 did not affect expression of either NR2A- or NR2B- containing NMDARs;however, it depressed the phosphorylation of the NR2B subunit at Ser-1303.These findings provide direct evidence that fast nongenomic neuroprotection by estradiol is mediated by gPR30 stimulation and ensuing down-regulation of NR2Bcontaining NMDARs.Modulation of NMDAR activity by gPR30 stimulation may be an important mediator of estradiol-dependent neuroprotection.

关键词： N-methyl-D-aspartate receptor g-protein-coupled receptor 30 neuroprotection

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Fast nongenomic neuroprotection mediated by gPR30-dependent depression of NR2B-containing NMDA receptors

Fast nongenomic neuroprotection mediated by GPR30-dependent ...

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中国神经科学学会第九届全国学术会议暨第五次会员代表大会

作者： Ming-gao ZHAO~* Department of Pharmacology,School of Pharmacy,Fourth Military Medical University,Xi''an 710032,China

＜正＞17-β-Estradiol（E2） is a steroid hormone involved in neuroprotection against excitotoxicity and other forms of brain injury.Throμgh genomic and non-genomic mechanisms,E2 modulates neuronal excitability and rapidly increases signal transmission by regulating N-methyl D-aspartate（NMDA） and non-NMDA receptors.The potential neuroprotective role of estradiol in chronic neurodegenerative disorders and acute brain ischemia following cardiac arrest and stroke is of great therapeutic interest.However,the mechanisms and identity of the receptors involved remain unclear,althoμgh it has been sμggested that g-protein-coupled receptor 30（gPR30） is linked to protection against ischemic insults.In this study,rapid nongenomic neuroprotection by gPR30 stimulation was examined in culture cortical neurons.Both E2 and the gPR30 agonist g1 attenuated the excitotoxicity induced by NMDA receptor stimulation.The acute neuroprotection induced by gPR30 stimulation was dependent on g-protein coupled signaling and ERK1/2 activation,but independent of gene transcription and protein synthesis.Knockdown of gPR30 by transfection with small interfering RNAs（siRNAs） significantly reduced E2-induced rapid neuro-protection.Patchclamp recordings revealed that the activation of gPR30 significantly depressed exogenous NMDA-elicited currents. Short-term activation of gPR30 did not affect expression of either NR2A- or NR2B-containing NMDARs;however, it depressed the phosphorylation of the NR2B subunit at Ser-1303.These findings provide direct evidence that fast nongenomic neuroprotection by estradiol is mediated by gPR30 stimulation and ensuing down-regulation of NR2B-containing NMDARs.Modulation of NMDAR activity by gPR30 stimulation may be an important mediator of estradiol-dependent neuroprotection.

关键词： N-methyl-D-aspartate receptor g-protein-coupled receptor 30 neuroprotection

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