scholarly journals Mechanisms governing dendritic gamma -aminobutyric acid (GABA) release in the rat olfactory bulb

2000 ◽  
Vol 98 (1) ◽  
pp. 337-342 ◽  
Author(s):  
J. S. Isaacson
Keyword(s):  
Olfactory Bulb ◽  
Gaba Release ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid

GABA release in posterior hypothalamus across sleep-wake cycle

1996 ◽  
Vol 271 (6) ◽  
pp. R1707-R1712 ◽  
Author(s):  
D. Nitz ◽  
J. M. Siegel
Keyword(s):  
Receptor Agonist ◽  
High Performance ◽  
Slow Wave Sleep ◽  
Gaba Release ◽  
Posterior Hypothalamus ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Rapid Eye Movement Sleep ◽  
Unit Discharge ◽  
Selective Increase

The activity of neurons in the posterior hypothalamus (PH) is thought to contribute to the production of wakefulness and electroencephalograph desynchronization. Inactivation of neuronal activity in this area is known to induce sleep. Most PH neurons decrease unit discharge during slow-wave sleep (SWS) relative to wake and rapid eye movement sleep. In the present study, we sought to examine potential sources of inhibition or disfacilitation underlying the reduction of PH unit activity during SWS in the cat. We employed the microdialysis technique in conjunction with high-performance liquid chromatography methods for the quantification of glutamate, glycine, and gamma-aminobutyric acid (GABA) release. We found a selective increase in GABA release during SWS in the PH. Glutamate and glycine levels were unchanged across the sleep-wake cycle. microinjection of the GABAA-receptor agonist muscimol, into the same areas from which microdialysis samples were collected, increased SWS time. Our studies support the hypothesis that GABA release in the posterior hypothalamus mediates inhibition of posterior hypothalamic neurons, thereby facilitating SWS.

Uptake and release of gamma-aminobutyric acid in guinea pig gallbladder

1985 ◽  
Vol 249 (2) ◽  
pp. G192-G196 ◽  
Author(s):  
N. Saito ◽  
K. Taniyama ◽  
C. Tanaka
Keyword(s):  
Guinea Pig ◽  
Ganglion Cells ◽  
Regional Distribution ◽  
Gaba Release ◽  
Aminobutyric Acid ◽  
Transport Systems ◽  
Gamma Aminobutyric Acid ◽  
Beta Alanine ◽  
High Affinity ◽  
Uptake And Release

The presence of gamma-aminobutyric acid (GABA)-ergic neuron in guinea pig gallbladder was investigated by measuring GABA contents and glutamate decarboxylase (GAD) activity and by demonstrating the uptake and release of [3H]GABA. GABA and GAD are both present in the gallbladder, and a positive correlation in regional distribution was observed among GABA, GAD, and the number of ganglion cells. The uptake of [3H]GABA by the gallbladder showed two saturable components; a high-affinity component (Km = 23.3 microM, Vmax = 7.63 nmol X g-1 X 10 min-1) and a low-affinity component (Km = 515 microM, Vmax = 57.1 nmol X g-1 X 10 min-1). These high-affinity and low-affinity transport systems corresponded to those obtained in the presence of beta-alanine and L-2,4-diaminobutyric acid, respectively, thereby suggesting the presence of neuronal and nonneuronal GABA transport systems in this tissue. Electrical transmural stimulation produced an increase in [3H]-GABA release from the isolated gallbladder preloaded with [3H]GABA, in the presence of beta-alanine. The stimulation-evoked release of [3H]GABA was prevented by calcium-free medium containing 1 mM EGTA and tetrodotoxin, thereby indicating that the released GABA originates from the nerve terminals. These results provide evidence for the presence of GABA-ergic neurons in the guinea pig gallbladder.

Halothane and Isoflurane Differentially Affect the Regulation of Dopamine and Gamma-aminobutyric Acid Release Mediated by Presynaptic Acetylcholine Receptors in the Rat Striatum

1997 ◽  
Vol 86 (3) ◽  
pp. 632-641 ◽  
Author(s):  
Francois Salord ◽  
Hawa Keita ◽  
Jean-Baptiste Lecharny ◽  
Danielle Henzel ◽  
Jean-Marie Desmonts ◽  
...  
Keyword(s):  
Potassium Chloride ◽  
Acetylcholine Receptors ◽  
Gaba Release ◽  
Volatile Anesthetics ◽  
Aminobutyric Acid ◽  
Rat Striatum ◽  
Gamma Aminobutyric Acid ◽  
General Anesthetics ◽  
Depolarizing Agents ◽  
Da Release

Background General anesthetics are thought to produce their hypnotic effects mainly by acting at ligand-gated ionic channels in the central nervous system (CNS). Although it is well established that volatile anesthetics significantly modify the activity of the acetylcholine nicotinic receptors of the neuromuscular junction, little is known about their actions on the acetylcholine receptors in the CNS. In this study, the effects of halothane and isoflurane on the regulation of dopamine (DA) (gamma-aminobutyric acid [GABA]) depolarization-evoked release mediated by nicotinic (muscarinic) presynaptic receptors were studied in the rat striatum. Methods Assay for GABA (dopamine) release consisted of 3H-GABA (3H-DA)-preloaded synaptosomes with artificial cerebrospinal fluid (0.5 ml/min, 37 degrees C) and measuring the radioactivity obtained from 1-min fractions for 18 min, first in the absence of any treatment (spontaneous release, 8 min), then in the presence of depolarizing agents combined with vaporized halothane and isoflurane (0.5-5%, 5 min), and finally with no pharmacologic stimulation (5 min). The depolarizing agents were potassium chloride (KCl; 9 mM) alone or with acetylcholine (10(-6)-10(-4) M) and/or atropine (10(-5) M) for experiments with 3H-GABA, and KC1 (15 mM) and nicotine (10(-7) - 5 x 10(-4) M) alone or with mecamylamine (10(-5) M) for experiments with 3H-DA. Results Potassium chloride induced a significant, Ca(2+)-dependent release of both 3H-GABA and 3H-DA. Nicotine produced a concentration-related, mecamylamine-sensitive 3H-DA release that was significantly attenuated by nicotine (10(-7) M) preincubation. Acetylcholine elicited a dose-dependent, atropine-sensitive reduction of the KC1-evoked 3H-GABA release. Halothane and isoflurane significantly decreased the nicotine-evoked 3H-DA release but had only limited depressant effects on the KC1-stimulated 3H-DA and no action on the KC1-induced 3H-GABA release. The effects of acetylcholine on 3H-GABA release were reversed by halothane but not by isoflurane. Conclusions Clinically relevant concentrations of halothane and isoflurane significantly, but differentially, alter the presynaptic cholinergic regulation of the release of inhibitory neurotransmitters in the striatum. These results suggest that the cholinergic transmission may represent an important and specific presynaptic target for volatile anesthetics in the CNS.

Regulation of [3H]GABA release from strips of guinea pig urinary bladder

1988 ◽  
Vol 255 (6) ◽  
pp. R888-R893
Author(s):  
J. Shirakawa ◽  
K. Taniyama ◽  
S. Iwai ◽  
C. Tanaka
Keyword(s):  
Urinary Bladder ◽  
Guinea Pig ◽  
Adrenergic Receptors ◽  
Gaba Release ◽  
Inhibitory Effect ◽  
Atropine Sulfate ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
High K ◽  
M1 Muscarinic

The presence of receptors that regulate the release of gamma-aminobutyric acid (GABA) was studied in strips of the guinea pig urinary bladder. GABA (10(-8)-10(-5) M) and muscimol (10(-8)-10(-5) M), but not baclofen (10(-5) M), reduced the Ca2+-dependent, tetrodotoxin-resistant release of [3H]GABA evoked by high K+ from the urinary bladder strips preloaded with [3H]GABA. The inhibitory effect of muscimol was antagonized by bicuculline and potentiated by diazepam, clonazepam, and pentobarbital sodium. The potentiating effect of clonazepam was antagonized by Ro 15-1788. Acetylcholine (ACh) inhibited the high K+-evoked release of [3H]GABA. The inhibitory effect of ACh was antagonized by atropine sulfate and pirenzepine but not by hexamethonium. Norepinephrine (NE) inhibited the evoked release of [3H]GABA. The inhibitory effect of NE was mimicked by clonidine, but not by phenylephrine, and was antagonized by yohimbine but not by prazosin. These results provide evidence that the release of GABA from strips of guinea pig urinary bladder is regulated via the bicuculline-sensitive GABAA receptor, M1-muscarinic, and alpha 2-adrenergic receptors.

Synapsin I Synchronizes GABA Release in Distinct Interneuron Subpopulations

2019 ◽  
Vol 30 (3) ◽  
pp. 1393-1406
Author(s):  
N Forte ◽  
F Binda ◽  
A Contestabile ◽  
F Benfenati ◽  
P Baldelli
Keyword(s):  
In Situ Hybridization ◽  
Patch Clamp ◽  
Action Potential ◽  
Hippocampal Slices ◽  
Gaba Release ◽  
Aminobutyric Acid ◽  
Synapsin I ◽  
Gamma Aminobutyric Acid ◽  
Asynchronous Release

Abstract Neurotransmitters can be released either synchronously or asynchronously with respect to action potential timing. Synapsins (Syns) are a family of synaptic vesicle (SV) phosphoproteins that assist gamma-aminobutyric acid (GABA) release and allow a physiological excitation/inhibition balance. Consistently, deletion of either or both Syn1 and Syn2 genes is epileptogenic. In this work, we have characterized the effect of SynI knockout (KO) in the regulation of GABA release dynamics. Using patch-clamp recordings in hippocampal slices, we demonstrate that the lack of SynI impairs synchronous GABA release via a reduction of the readily releasable SVs and, in parallel, increases asynchronous GABA release. The effects of SynI deletion on synchronous GABA release were occluded by ω-AgatoxinIVA, indicating the involvement of P/Q-type Ca2+channel-expressing neurons. Using in situ hybridization, we show that SynI is more expressed in parvalbumin (PV) interneurons, characterized by synchronous release, than in cholecystokinin or SOM interneurons, characterized by a more asynchronous release. Optogenetic activation of PV and SOM interneurons revealed a specific reduction of synchronous release in PV/SynIKO interneurons associated with an increased asynchronous release in SOM/SynIKO interneurons. The results demonstrate that SynI is differentially expressed in interneuron subpopulations, where it boosts synchronous and limits asynchronous GABA release.

scholarly journals The Role of GAD65 Autoantibodies in the development of Type-1 Diabetes

2021 ◽  
Vol 36 (3) ◽  
pp. 103-106
Author(s):  
Sri R. Prasetyo
Keyword(s):  
Type 1 Diabetes ◽  
B Cells ◽  
Islet Cells ◽  
Gaba Release ◽  
Fine Tuning ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Key Enzyme ◽  
Type 1Diabetes

AbstractThe finding of the autoantibodies to islet cells (ICAs) in type-1 diabetes patients is important for developing the fine tuning of individualized therapy. Antibody to Glutamate decarboxylase 2 (GAD65Ab) is the most reliable sign, since it has the most stable sensitivity as diagnostic tool for detecting type-1diabetes. As a key enzyme in gamma-Aminobutyric acid (GABA) synthesis, GAD65 damage caused by GAD65 antibodies (GAD65Abs) would lead to decrease in the amount of GABA vesicles released by b-cells. Decrease of GAD65 induced by GAD65Ab may endanger the paracrine or autocrine function of GABA, that mediated by γ-aminobutyric acid type A receptors (GABAAR) would depolarized the b-cells. The depolarization then increases intracellular Calsium (Ca2+) concentration that is needed for insulin release. The effect of GABA on b-cells is also important for proliferation and anti-apoptosis of b-cells. Moreover, decrease in GABA release also impairs the inhibiting effect of GABA on T-cell proliferation and inflammatory cytokines release that may end up with escalation of GAD65 damage.Keywords: Type-1 diabetes, autoantibody, GAD65Peran Autoantibodi GAD65 dalam Perkembangan Diabetes Tipe-1AbstractPenemuan autoantibodi terhadap sel pulau atau islet cells (ICA) pada pasien diabetes tipe-1 penting untuk mengembangkan penyesuaian terapi individual. Antibodi terhadap Glutamat dekarboksilase 2 (GAD65Ab) adalah tanda yang paling dapat diandalkan, karena memiliki sensitivitas yang paling stabil sebagai alat diagnostik untuk mendeteksi diabetes tipe-1. Sebagai enzim kunci dalam sintesis asam gamma-aminobutirat (GABA), kerusakan GAD65 yang disebabkan oleh antibodi GAD65 (GAD65Abs) akan menyebabkan penurunan jumlah vesikel GABA yang dilepaskan oleh sel. Penurunan GAD65 yang diinduksi oleh GAD65Ab dapat membahayakan fungsi parakrin atau autokrin GABA, yang dimediasi oleh reseptor asam γ-aminobutirat tipe A (GABAAR) akan mendepolarisasi sel. Depolarisasi kemudian meningkatkan konsentrasi kalsium (Ca2+) intraseluler yang diperlukan untuk pelepasan insulin. Efek GABA pada sel beta juga penting untuk proliferasi dan anti-apoptosis sel beta. Selain itu, penurunan pelepasan GABA juga merusak efek penghambatan GABA pada proliferasi sel T dan pelepasan sitokin inflamasi yang mungkin berakhir dengan peningkatan kerusakan GAD65.Kata kunci: Diabetes tipe-1, autoantibodi, GAD65

Release of endogenous and labeled GABA from isolated guinea pig ileum

1983 ◽  
Vol 245 (5) ◽  
pp. G717-G721 ◽  
Author(s):  
K. Taniyama ◽  
Y. Miki ◽  
M. Kusunoki ◽  
N. Saito ◽  
C. Tanaka
Keyword(s):  
Guinea Pig ◽  
Gaba Release ◽  
Ringer Solution ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Tetraacetic Acid ◽  
Spontaneous Release ◽  
Guinea Pig Ileum ◽  
Fractional Rate ◽  
Endogenous Gaba

The release of gamma-aminobutyric acid (GABA) was studied by comparing the properties of labeled GABA released from preloaded preparations to those of endogenous GABA released from the isolated guinea pig ileum. The spontaneous release of endogenous GABA was 4.46 +/- 0.10 pmol X min-1 X g wet wt-1, and the fractional rate of endogenous GABA release was much lower. The ratio of evoked to spontaneous release of endogenous GABA was high compared with that of labeled GABA. The electrical transmural stimulation-evoked release of labeled and endogenous GABA was inhibited by superfusion with tetrodotoxin and Ca2+-free Krebs-Ringer solution containing 1 mM ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid. Thus the nature of the stimulation-evoked release of labeled GABA was similar to that of endogenous GABA. These results indicate that the released GABA is neuronal in origin and provide additional evidence for the presence of GABA-ergic neurons in the guinea pig ileum.

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