scholarly journals Neurochemical studies on γ-aminobutyric acid(GABA) receptor (XXXVI). Presynaptic regulation of GABA release from GABA terminal: Analysis using in vivo microdialysis.

1993 ◽  
Vol 61 ◽  
pp. 153
Author(s):  
Tsuneichi Hashimoto ◽  
Kinya Kuriyama
Keyword(s):  
Gaba Receptor ◽  
Gaba Release ◽  
In Vivo Microdialysis ◽  
Aminobutyric Acid ◽  
Presynaptic Regulation

Avermectin and avermectin derivatives are antagonists at the 4-aminobutyric acid (GABA) receptor on the somatic muscle cells of Ascaris; is this the site of anthelmintic action?

Parasitology ◽  
1990 ◽  
Vol 101 (2) ◽  
pp. 265-271 ◽  
Author(s):  
L. Dye-Holden ◽  
R. J. Walker
Keyword(s):  
Receptor Antagonist ◽  
Gaba Receptor ◽  
Parasitic Nematode ◽  
Anthelmintic Activity ◽  
Muscle Cells ◽  
Aminobutyric Acid ◽  
Electrophysiological Recording ◽  
Receptor Antagonists ◽  
Somatic Muscle

The mechanism underlying the ability of the anthelmintic avermectin to paralyse the nematode Ascaris is not yet fully understood. Using conventional two-electrode electrophysiological recording techniques we have demonstrated that micromolar concentrations of ivermectin block the inhibitory GABA response on the muscle cells of the parasitic nematode Ascaris. The ability of a number of avermectin derivatives to act as receptor antagonists for the Ascaris muscle GABA receptor has been determined. This provides useful information to compare with the in vivo anthelmintic potency of these compounds. Abamectin, the most potent anthelmintic, was the most potent compound at inhibiting the GABA response whilst octahydroavermectin, a compound which lacks anthelmintic activity, did not block the GABA receptor. This is consistent with the notion that the GABA receptor antagonist properties of the avermectins could contribute to their anthelmintic action.

scholarly journals Control of motor coordination by astrocytic tonic GABA release through modulation of excitation/inhibition balance in cerebellum

2018 ◽  
Vol 115 (19) ◽  
pp. 5004-5009 ◽  
Author(s):  
Junsung Woo ◽  
Joo Ok Min ◽  
Dae-Si Kang ◽  
Yoo Sung Kim ◽  
Guk Hwa Jung ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Motor Performance ◽  
Neuronal Excitability ◽  
Motor Coordination ◽  
Granule Cells ◽  
Cerebellar Granule Cells ◽  
Gaba Release ◽  
In Vivo Microdialysis ◽  
Tonic Inhibition

Tonic inhibition in the brain is mediated through an activation of extrasynaptic GABAA receptors by the tonically released GABA, resulting in a persistent GABAergic inhibitory action. It is one of the key regulators for neuronal excitability, exerting a powerful action on excitation/inhibition balance. We have previously reported that astrocytic GABA, synthesized by monoamine oxidase B (MAOB), mediates tonic inhibition via GABA-permeable bestrophin 1 (Best1) channel in the cerebellum. However, the role of astrocytic GABA in regulating neuronal excitability, synaptic transmission, and cerebellar brain function has remained elusive. Here, we report that a reduction of tonic GABA release by genetic removal or pharmacological inhibition of Best1 or MAOB caused an enhanced neuronal excitability in cerebellar granule cells (GCs), synaptic transmission at the parallel fiber-Purkinje cell (PF-PC) synapses, and motor performance on the rotarod test, whereas an augmentation of tonic GABA release by astrocyte-specific overexpression of MAOB resulted in a reduced neuronal excitability, synaptic transmission, and motor performance. The bidirectional modulation of astrocytic GABA by genetic alteration of Best1 or MAOB was confirmed by immunostaining and in vivo microdialysis. These findings indicate that astrocytes are the key player in motor coordination through tonic GABA release by modulating neuronal excitability and could be a good therapeutic target for various movement and psychiatric disorders, which show a disturbed excitation/inhibition balance.

scholarly journals Evidence that γ-Aminobutyric Acid Is Part of the Neural Circuit Mediating Estradiol Negative Feedback in Anestrous Ewes

Endocrinology ◽  
2008 ◽  
Vol 149 (6) ◽  
pp. 2762-2772 ◽  
Author(s):  
Adrienne L. Bogusz ◽  
Steven L. Hardy ◽  
Michael N. Lehman ◽  
John M. Connors ◽  
Stanley M. Hileman ◽  
...  
Keyword(s):  
Negative Feedback ◽  
Gaba Receptor ◽  
Receptor Agonist ◽  
Neural Circuit ◽  
Gabab Receptor ◽  
Gaba Release ◽  
Aminobutyric Acid ◽  
Receptor Ligands ◽  
Endogenous Gaba ◽  
Lh Secretion

Seasonal anestrus in ewes is driven by an increase in response to estradiol (E2) negative feedback. Compelling evidence indicates that inhibitory A15 dopaminergic (DA) neurons mediate the increased inhibitory actions of E2 in anestrus, but these neurons do not contain estrogen receptors. Therefore, we have proposed that estrogen-responsive afferents to A15 neurons are part of the neural circuit mediating E2 negative feedback in anestrus. This study examined the possible role of afferents containing γ-aminobutyric acid (GABA) and nitric oxide (NO) in modulating the activity of A15 neurons. Local administration of NO synthase inhibitors to the A15 had no effect on LH, but GABA receptor ligands produced dramatic changes. Administration of either a GABAA or GABAB receptor agonist to the A15 increased LH secretion in ovary-intact ewes, suggesting that GABA inhibits A15 neural activity. In ovariectomized anestrous ewes, the same doses of GABA receptor agonist had no effect, but combined administration of a GABAA and GABAB receptor antagonist to the A15 inhibited LH secretion. These data are consistent with the hypothesis that endogenous GABA release within the A15 is low in ovary-intact anestrous ewes and elevated after ovariectomy. Using dual immunocytochemistry, we observed that GABAergic varicosities make close contacts on to A15 neurons and that A15 neurons contain both the GABAA-α1 and the GABAB-R1 receptor subunits. Based on these data, we propose that in anestrous ewes, E2 inhibits release of GABA from afferents to A15 DA neurons, increasing the activity of these DA neurons and thus suppressing episodic secretion of GnRH and LH.

scholarly journals Effect of corticotropin-releasing factor on GABA release in rat hypothalamus assessed by in vivo microdialysis

1995 ◽  
Vol 67 ◽  
pp. 232
Author(s):  
Miho Matsui ◽  
Hiroyuki Emoto ◽  
Hideyasu Yokoo ◽  
Masami Yoshida ◽  
Takahiko Tanaka ◽  
...  
Keyword(s):  
Gaba Release ◽  
In Vivo Microdialysis ◽  
Corticotropin Releasing Factor ◽  
Rat Hypothalamus

Role of GABA within the nucleus tractus solitarii in the hypoxic ventilatory decline of awake rats

2001 ◽  
Vol 281 (5) ◽  
pp. R1411-R1419 ◽  
Author(s):  
Masao Tabata ◽  
Hajime Kurosawa ◽  
Yoshihiro Kikuchi ◽  
Wataru Hida ◽  
Hiromasa Ogawa ◽  
...  
Keyword(s):  
In Vivo Microdialysis ◽  
Nucleus Tractus Solitarii ◽  
Aminobutyric Acid ◽  
Hypoxic Exposure ◽  
Gaba Concentration ◽  
Gaba Agonists ◽  
Freely Moving ◽  
Gaba Agonists And Antagonists

The purpose of this study was to examine our hypothesis that γ-aminobutyric acid (GABA) in the nucleus tractus solitarii (NTS) may be related to the hypoxic ventilatory decline (HVD) and that chemoreceptor stimulation was essential to activate this mechanism. We used unanesthetized, freely moving rats in this study. An in vivo microdialysis technique was used to measure the extracellular GABA concentration ([GABA]o), and an in vivo microinjection technique was used to examine the effects of the GABA agonists and antagonists on the ventilation during hypoxia. The GABA agonists injected into the NTS attenuated the ventilation during hypoxia. By hypoxic exposure, [GABA]o was increased during the HVD. However, by carotid body denervation (CBD), this GABA increase was abolished. Although GABA antagonists microinjected into the NTS during the HVD phase significantly increased the depressed ventilation, this effect on the ventilation was abolished by CBD. These results suggest that the GABA in the NTS has a pivotal role in the HVD and that this mechanism is not activated without chemoreceptor stimulation.

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