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.

Autoradiographic Localization of the Gamma-Aminobutyric Acid Type A Receptor Agonist 3H-Muscimol in the Rat Superior Cervical Ganglion

Pharmacology ◽  
1992 ◽  
Vol 44 (2) ◽  
pp. 107-112 ◽  
Author(s):  
Francesco Amenta ◽  
Elena Bronzetti ◽  
Carlo Cavallotti ◽  
Laura Felici ◽  
Fabio Ferrante ◽  
...  
Keyword(s):  
Superior Cervical Ganglion ◽  
Receptor Agonist ◽  
Type A ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Acid Type ◽  
Cervical Ganglion

scholarly journals Optimization of Gamma Aminobutyric Acid Production Using High Pressure Processing (HPP) by Lactobacillus brevis PML1

2022 ◽  
Vol 2022 ◽  
pp. 1-9
Author(s):  
Atefe Ghafurian Nasab ◽  
Sayed Ali Mortazavi ◽  
Farideh Tabatabaei Yazdi ◽  
Mahboobe Sarabi Jamab
Keyword(s):  
High Performance ◽  
Morphological Changes ◽  
Control Sample ◽  
Bioactive Compound ◽  
Lactobacillus Brevis ◽  
High Pressure Processing ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Viability Analysis ◽  
Layer Chromatography

In the present research, the production potential of gamma aminobutyric acid (GABA) using Lactobacillus brevis PML1 was investigated. In addition, the microorganism viability was examined in MAN, ROGOSA, and SHARPE (MRS) after undergoing high hydrostatic pressure at 100, 200, and 300 MPa for 5, 10, and 15 min. Response surface methodology (RSM) was applied to optimize the production conditions of GABA as well as the bacteria viability. Analysis of variance (ANOVA) indicated that both the independent variables (pressure and time) significantly influenced the dependent ones (GABA and bacteria viability) ( P < 0.05 ). The optimum extraction conditions to maximize the production of GABA included the pressure of 300 MPa and the time of 15 min. The amount of the compound was quantified using thin-layer chromatography (TLC) and spectrophotometry. For the process optimization, a central composite design (CCD) was created using Design Expert with 5 replications at the center point, whereby the highest content of GABA was obtained to be 397.73 ppm which was confirmed by high performance liquid chromatography (HPLC). Moreover, scanning electron microscopy (SEM) was utilized to observe the morphological changes in the microorganism. The results revealed that not only did have Lactobacillus brevis PML1 the potential for the production of GABA under conventional conditions (control sample) but also the content of this bioactive compound could be elevated by optimizing the production parameters.

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 Activation of Nigral and Pallidal Dopamine D1-Like Receptors Modulates Basal Ganglia Outflow in Monkeys

2007 ◽  
Vol 98 (3) ◽  
pp. 1489-1500 ◽  
Author(s):  
Michele A. Kliem ◽  
Nigel T. Maidment ◽  
Larry C. Ackerson ◽  
Sugong Chen ◽  
Yoland Smith ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Rhesus Monkeys ◽  
Receptor Agonist ◽  
Gaba Release ◽  
Aminobutyric Acid ◽  
Substantia Nigra Pars Reticulata ◽  
Axon Terminals ◽  
Discharge Rates ◽  
Dopaminergic Tone ◽  
Output Neurons

Studies of the effects of dopamine in the basal ganglia have focused on the striatum, whereas the functions of dopamine released in the internal pallidal segment (GPi) or in the substantia nigra pars reticulata (SNr) have received less attention. Anatomic and biochemical investigations have demonstrated the presence of dopamine D1-like receptors (D1LRs) in GPi and SNr, which are primarily located on axons and axon terminals of the GABAergic striatopallidal and striatonigral afferents. Our experiments assessed the effects of D1LR ligands in GPi and SNr on local γ-aminobutyric acid (GABA) levels and neuronal activity in these nuclei in rhesus monkeys. Microinjections of the D1LR receptor agonist SKF82958 into GPi and SNr significantly reduced discharge rates in GPi and SNr, whereas injections of the D1LR antagonist SCH23390 increased firing in the majority of GPi neurons. D1LR activation also increased bursting and oscillations in neuronal discharge in the 3- to 15-Hz band in both structures, whereas D1LR blockade had the opposite effects in GPi. Microdialysis measurements of GABA concentrations in GPi and SNr showed that the D1LR agonist increased the level of the transmitter. Both findings are compatible with the hypothesis that D1LR activation leads to GABA release from striatopallidal or striatonigral afferents, which may secondarily reduce firing of basal ganglia output neurons. The antagonist experiments suggest that a dopaminergic “tone” exists in GPi. Our results support the finding that D1LR activation may have powerful effects on GPi and SNr neurons and may mediate some of the effects of dopamine replacement therapies in Parkinson's disease.

Regulation of endogenous dopamine release in amphibian retina by gamma-aminobutyric acid and glycine

1994 ◽  
Vol 11 (5) ◽  
pp. 1003-1012 ◽  
Author(s):  
Jeffrey H. Boatright ◽  
Nara M. Rubim ◽  
P. Michael Iuvone
Keyword(s):  
Receptor Agonist ◽  
Dopamine Release ◽  
Receptor Activation ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Gaba A ◽  
Endogenous Dopamine ◽  
Endogenous Dopamine Release ◽  
Inhibitory Tone

AbstractEndogenous dopamine release in the retina of the African clawed frog (Xenopus laevis) increases in light and decreases in darkness. The roles of the inhibitory amino acid transmitters gamma-aminobutyric acid (GABA) and glycine in regulating this light/dark difference in dopamine release were explored in the present study. Exogenous GABA, the GABA-A receptor agonist muscimol, the GABA-B receptor agonist baclofen, and the GABA-C receptor agonist cis-aminocrotonic acid (CACA) suppressed light-evoked dopamine overflow from eyecups. The effects of GABA-A and -B receptor agonists were selectively reversed by their respective receptor-specific antagonists, whereas the effect of CACA was reversed by the competitive GABA-A receptor antagonist bicuculline. The benzodiazepine diazepam enhanced the effect of muscimol on light-evoked dopamine release. Both GABA-A and -B receptor antagonists stimulated dopamine release in light or darkness. Bicuculline was more potent in light than in darkness. These data suggest that retinal dopaminergic neurons are inhibited by GABA-A and -B receptor activation in both light and darkness but that GABA-mediated inhibitory tone may be greater in darkness than in light.Exogenous glycine inhibited light-stimulated dopamine release in a concentration-dependent and strychnine-sensitive manner. However, strychnine alone did not increase dopamine release in light or darkness, nor did it augment bicuculline-stimulated release in darkness. Additionally, both strychnine and 7-chlorokynurenate, an antagonist of the strychnine-insensitive glycine-binding site of the N-methyl-D-aspartate subtype of glutamate receptor, suppressed light-evoked dopamine release. Thus, the role of endogenous glycine in the regulation of dopamine release remains unclear.

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