Brain hydrogen sulfide suppresses the micturition reflex via brain GABA receptors in rats

Nitric Oxide ◽  
2020 ◽  
Vol 104-105 ◽  
pp. 44-50
Author(s):  
Masaki Yamamoto ◽  
Takahiro Shimizu ◽  
Suo Zou ◽  
Shogo Shimizu ◽  
Youichirou Higashi ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Gaba Receptors ◽  
Micturition Reflex ◽  
Brain Gaba

scholarly journals MP08-03 BRAIN HYDROGEN SULFIDE SUPPRESSES THE RAT MICTURITION REFLEX VIA BRAIN GABA RECEPTORS

2021 ◽  
Vol 206 (Supplement 3) ◽  
Author(s):  
Masaki Yamamoto ◽  
Takahiro Shimizu ◽  
Suo Zou ◽  
Shogo Shimizu ◽  
Youichirou Higashi ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Gaba Receptors ◽  
Micturition Reflex ◽  
Brain Gaba

Effects of learned helplessness on brain GABA receptors

2000 ◽  
Vol 38 (2) ◽  
pp. 193-198 ◽  
Author(s):  
Martin L Kram ◽  
Gerald L Kramer ◽  
Mark Steciuk ◽  
Patrick J Ronan ◽  
Frederick Petty
Keyword(s):  
Learned Helplessness ◽  
Gaba Receptors ◽  
Brain Gaba

scholarly journals Electrophysiology of ionotropic GABA receptors

2021 ◽  
Author(s):  
Erwan Sallard ◽  
Diane Letourneur ◽  
Pascal Legendre
Keyword(s):  
Electrical Activity ◽  
Gaba Receptors ◽  
Chloride Channels ◽  
Expression Patterns ◽  
Cell Types ◽  
Inhibitory Neurotransmitter ◽  
Electrophysiological Properties ◽  
Neuronal Communication ◽  
External Signals ◽  
Brain Gaba

AbstractGABAA receptors are ligand-gated chloride channels and ionotropic receptors of GABA, the main inhibitory neurotransmitter in vertebrates. In this review, we discuss the major and diverse roles GABAA receptors play in the regulation of neuronal communication and the functioning of the brain. GABAA receptors have complex electrophysiological properties that enable them to mediate different types of currents such as phasic and tonic inhibitory currents. Their activity is finely regulated by membrane voltage, phosphorylation and several ions. GABAA receptors are pentameric and are assembled from a diverse set of subunits. They are subdivided into numerous subtypes, which differ widely in expression patterns, distribution and electrical activity. Substantial variations in macroscopic neural behavior can emerge from minor differences in structure and molecular activity between subtypes. Therefore, the diversity of GABAA receptors widens the neuronal repertoire of responses to external signals and contributes to shaping the electrical activity of neurons and other cell types.

scholarly journals Brain α7 nicotinic receptor stimulation inhibits the rat micturition reflex via brain GABAA receptors

2021 ◽  
Vol 94 (0) ◽  
pp. 2-P2-20
Author(s):  
Yohei Shimizu ◽  
Takahiro Shimizu ◽  
Hideaki Ono ◽  
Suo Zou ◽  
Masaki Yamamoto ◽  
...  
Keyword(s):  
Nicotinic Receptor ◽  
Receptor Stimulation ◽  
Micturition Reflex ◽  
Brain Gaba

Endogenous hydrogen sulfide sulfhydrates IKKβ at cysteine 179 to control pulmonary artery endothelial cell inflammation

2019 ◽  
Vol 133 (20) ◽  
pp. 2045-2059 ◽  
Author(s):  
Da Zhang ◽  
Xiuli Wang ◽  
Siyao Chen ◽  
Selena Chen ◽  
Wen Yu ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Endothelial Cell ◽  
Pulmonary Artery ◽  
Cell Model ◽  
Site Directed Mutagenesis ◽  
Critical Event ◽  
Hypertensive Rats ◽  
Pulmonary Artery Endothelial Cell

Abstract Background: Pulmonary artery endothelial cell (PAEC) inflammation is a critical event in the development of pulmonary arterial hypertension (PAH). However, the pathogenesis of PAEC inflammation remains unclear. Methods: Purified recombinant human inhibitor of κB kinase subunit β (IKKβ) protein, human PAECs and monocrotaline-induced pulmonary hypertensive rats were employed in the study. Site-directed mutagenesis, gene knockdown or overexpression were conducted to manipulate the expression or activity of a target protein. Results: We showed that hydrogen sulfide (H2S) inhibited IKKβ activation in the cell model of human PAEC inflammation induced by monocrotaline pyrrole-stimulation or knockdown of cystathionine γ-lyase (CSE), an H2S generating enzyme. Mechanistically, H2S was proved to inhibit IKKβ activity directly via sulfhydrating IKKβ at cysteinyl residue 179 (C179) in purified recombinant IKKβ protein in vitro, whereas thiol reductant dithiothreitol (DTT) reversed H2S-induced IKKβ inactivation. Furthermore, to demonstrate the significance of IKKβ sulfhydration by H2S in the development of PAEC inflammation, we mutated C179 to serine (C179S) in IKKβ. In purified IKKβ protein, C179S mutation of IKKβ abolished H2S-induced IKKβ sulfhydration and the subsequent IKKβ inactivation. In human PAECs, C179S mutation of IKKβ blocked H2S-inhibited IKKβ activation and PAEC inflammatory response. In pulmonary hypertensive rats, C179S mutation of IKKβ abolished the inhibitory effect of H2S on IKKβ activation and pulmonary vascular inflammation and remodeling. Conclusion: Collectively, our in vivo and in vitro findings demonstrated, for the first time, that endogenous H2S directly inactivated IKKβ via sulfhydrating IKKβ at Cys179 to inhibit nuclear factor-κB (NF-κB) pathway activation and thereby control PAEC inflammation in PAH.

Sign in / Sign up

Export Citation Format

Share Document