No abstract available.
gamma-Aminobutyric Acid* ; Nervous System* ; Receptors, GABA*

No abstract available.
Benzodiazepines* ; gamma-Aminobutyric Acid* ; Receptors, GABA-A*

No abstract available.
Amines ; Cyclohexanecarboxylic Acids ; gamma-Aminobutyric Acid ; Hiccup

No abstract available.
Adenosine Triphosphatases* ; Animals ; Brain* ; gamma-Aminobutyric Acid* ; Phenytoin* ; Rats*

Gamma-aminobutyric acid (GABA) is an inhibitory neurotransmitter in the adult central nervous system (CNS), however, it causes excitation in the immature CNS neurons. The shift from GABA-induced depolarization to hyperpolarization in postnatal brain is primarily due to progressive decrease in the expression of the Na-K-2Cl symporter 1 (NKCC1) and increased expression of the K-Cl cotransporter 2 (KCC2). Unlike CNS neurons, both immature and mature neurons in the enteric nervous system (ENS) are depolarized by GABA. Molecular mechanisms by which GABA excites ENS neurons are unclear. It is understood, however, that the excitatory action depends on elevated intraneuronal Cl. We aimed to test a hypothesis that high intracellular Cl in ENS neurons is maintained by activity of the NKCCs. We found that NKCC2 immunoreactivity (IR) was expressed in the ENS of the rat colon on postnatal day 1 (P1). The expression level of NKCC2 continuously increased and reached a steady high level on P14 and maintained at that level in adulthood. NKCC1 IR appeared in ENS on P14 and maintained through adulthood. KCC2 IR was not detectable in the ENS in any of the developmental stages. Both NKCC1 IR and NKCC2 IR were co-expressed with GABA receptors in ENS neurons. Exogenous GABA (1 mmol/L) caused membrane depolarization in the ENS neurons. The reversal potential of GABA-induced depolarization was about -16 mV. Blockade of NKCC by bumetanide (50 μmol/L) or furosemide (300 μmol/L) suppressed the depolarizing responses to GABA. Bumetanide (50 μmol/L) shifted the reversal potential of GABA-induced depolarization in the hyperpolarizing direction. Neither the KCC blocker DIOA (20 μmol/L) nor the Cl/HCO exchanger inhibitor DIDS (200 μmol/L) suppressed GABA-evoked depolarization. The results suggest that ENS neurons continuously express NKCC2 since P1 and NKCC1 since P14, which contribute to the accumulation of Cl in ENS neurons and GABA-evoked depolarization in neonate and adult ENS neurons. These results provide the first direct evidence for the contribution of both NKCC2 and NKCC1 to the GABA-mediated depolarization.
Animals ; Bumetanide ; Neurons ; Rats ; Receptors, GABA-A ; Symporters ; gamma-Aminobutyric Acid

A rapid, sensitive and convenient LC-MS/MS method was developed for the determination of γ-aminobutyric acid (GABA) in human plasma. d2-γ-Aminobutyric acid (d2-GABA) was synthesized as internal standard (IS). After extraction from human plasma by protein precipitation with acetonitrile, all analytes were separated on a Luna HILIC column (100 mm x 3.0 mm, 3 μm) using an isocratic mobile phase of water: acetonitrile: formic acid (20 : 80 : 0.12) with a flow rate of 0.5 mL x min(-1). Acquisition of mass spectrometric data was performed in multiple reaction monitoring mode (MRM) in positive electrospray ionization using the transitions of m/z 104 --> 69 for GABA and m/z 106 --> 71 for d2-GABA. The method was linear in the concentration range of 5.00 to 1 000 ng x mL(-1). The intra- and inter-day precisions were within 9.9%, and accuracy ranged from 99.1% to 104%, within the acceptable limit across all concentrations. The method was successfully applied to a pharmacokinetic study of GABA tablets in healthy Chinese volunteers.
Chromatography, Liquid ; Humans ; Tandem Mass Spectrometry ; gamma-Aminobutyric Acid ; blood

This study was done to produce γ-aminobutyric acid (GABA) from wild yeast as well as investigate its anti-hyperglycemic effects. Among ten GABA-producing yeast strains, Pichia silvicola UL6-1 and Sporobolomyces carnicolor 402-JB-1 produced high GABA concentration of 134.4 µg/mL and 179.2 µg/mL, respectively. P. silvicola UL6-1 showed a maximum GABA yield of 136.5 µg/mL and 200.8 µg/mL from S. carnicolor 402-JB-1 when they were cultured for 30 hr at 30℃ in yeast extract-peptone-dextrose medium. The cell-free extract from P. silvicola UL6-1 and S. carnicolor 402-JB-1 showed very high anti-hyperglycemic α-glucosidase inhibitory activity of 72.3% and 69.9%, respectively. Additionally, their cell-free extract-containing GABA showed the anti-hyperglycemic effect in streptozotocin-induced diabetic Sprague-Dawley rats.
gamma-Aminobutyric Acid ; Pichia* ; Rats, Sprague-Dawley ; Yeasts*

PURPOSE: To evaluate the spatial distribution of various proton metabolites in the human brain with use of water-suppressed in vivo 1H MR spectroscopic imaging (MRSI) technique MATERIALS AND METHODS: All of water-suppressed in vivo 1H MRSI were performed on 1.5 T whole-body MRI/MRS system using Stimulated Echo Acquisition Method (STEAM) Chemical shift Imaging (CSI) pulse sequence. T1 -weighted MR images were used for CSl Field Of View (FOV; 24 cm). Voxel size of 1.S cm3 was designated from the periphery of the brain which was divided by 1024 x 16 x 16data points. RESULTS: Metabolite images of N-acetylaspartate (NAA), creatine/phosphocreatine (Cr) + choline/phosphocholine (Cho), and complex of gamma-aminobutyric acid (GABA) -I- glutamate (Glu) were obtained on the human brain. CONCLUSION: Our preliminary study suggests that in vivo 1H MRSl could provide the metabolite imaging to compensate for hypermetabolism on Positron Emission Tomography (PET) scans on the basis of the metabolic informations on brain tissues. The unique ability of in vivo 1H MRSI to offer noninvasive informations about tissue biochemistry in disease states will stimulate on clinical research and disease diagnosis.
Biochemistry ; Brain* ; Diagnosis ; gamma-Aminobutyric Acid ; Glutamic Acid ; Humans* ; Magnetic Resonance Imaging ; Positron-Emission Tomography ; Protons

The aim of this study was to examine the effects of various concentrations of glutamate(10(-8), 10(-6) and 10(-4) M) on the circling movement induced by apomorphine in the unilateral substantia nigra-lesioned rats. Subcutaneous apomorphine(0.1 mg/kg) elicited contralateral circling movement(641.7+/-163.9/hr), Glutamate(10(-6)-10(-4) M) significantly reduced the numbers of apomorphine-induced circling movement. This reducing effect of glutamate was antagonized and/or reversed by 10(-7) M GABA antagonist bicuculline. These results suggest that glutamate reduces circling movement induced by apomorphine and this reducing effect of glutamate may be mediated by increased GABA concentration in striatum and substantia nigra.
Animals ; Apomorphine ; Bicuculline ; Dopamine ; GABA Antagonists ; gamma-Aminobutyric Acid ; Glutamic Acid* ; Rats* ; Substantia Nigra

The etiology and pathogenesis of autism spectrum disorder (ASD) are not yet clear. Studies have shown that there are many neurotransmitter abnormalities in children with ASD, mainly involving in glutamate, γ-aminobutyric acid (GABA), dopamine, 5-HT and oxytocin. The imbalance of excitatory glutamatergic neurotransmitters and inhibitory GABAergic neurotransmitters is closely related to the pathogenesis of ASD. Both animal model studies and clinical studies on ASD suggest that GABA signaling pathway may play an important role in the pathogenesis of ASD. This article reviews the research on the association between GABA signaling pathway and the pathogenesis of ASD to further explore the pathogenesis of ASD and provide theoretical basis for the treatment of ASD.
Animals ; Autism Spectrum Disorder ; Disease Models, Animal ; Glutamic Acid ; Humans ; Signal Transduction ; gamma-Aminobutyric Acid