scholarly journals Multiple sources of internal calcium stores mediate ethanol-induced presynaptic inhibitory GABA release in the central nucleus of the amygdala in mice

2020 ◽  
Vol 237 (11) ◽  
pp. 3303-3314
Author(s):  
Qiang Li ◽  
Rebecca C. Klein ◽  
Scott D. Moore
Keyword(s):  
Gaba Release ◽  
Central Nucleus ◽  
Calcium Stores ◽  
Multiple Sources ◽  
Internal Calcium

scholarly journals Alcohol dependence potentiates substance P/neurokinin-1 receptor signaling in the rat central nucleus of amygdala

2020 ◽  
Vol 6 (12) ◽  
pp. eaaz1050
Author(s):  
S. Khom ◽  
T. Steinkellner ◽  
T. S. Hnasko ◽  
M. Roberto
Keyword(s):  
Substance P ◽  
Alcohol Dependence ◽  
Critical Role ◽  
Alcohol Exposure ◽  
Gaba Release ◽  
Central Nucleus ◽  
Neurokinin 1 Receptor ◽  
Neurokinin 1 ◽  
Gaba Transmission ◽  
Alcohol Dependent

Behavioral and clinical studies suggest a critical role of substance P (SP)/neurokinin-1 receptor (NK-1R) signaling in alcohol dependence. Here, we examined regulation of GABA transmission in the medial subdivision of the central amygdala (CeM) by the SP/NK-1R system, and its neuroadaptation following chronic alcohol exposure. In naïve rats, SP increased action potential–dependent GABA release, and the selective NK-1R antagonist L822429 decreased it, demonstrating SP regulation of CeM activity under basal conditions. SP induced a larger GABA release in alcohol-dependent rats accompanied by decreased NK-1R expression compared to naïve controls, suggesting NK-1R hypersensitivity which persisted during protracted alcohol withdrawal. The NK-1R antagonist blocked acute alcohol-induced GABA release in alcohol-dependent and withdrawn but not in naïve rats, indicating that dependence engages the SP/NK-1R system to mediate acute effects of alcohol. Collectively, we report long-lasting CeA NK-1R hypersensitivity corroborating that NK-1Rs are promising targets for the treatment of alcohol use disorder.

scholarly journals Oxidative stress increases internal calcium stores and reduces a key mitochondrial enzyme

2002 ◽  
Vol 1586 (2) ◽  
pp. 177-189 ◽  
Author(s):  
Gary E. Gibson ◽  
Hui Zhang ◽  
Hui Xu ◽  
Larry C.H. Park ◽  
Thomas M. Jeitner
Keyword(s):  
Oxidative Stress ◽  
Calcium Stores ◽  
Mitochondrial Enzyme ◽  
Internal Calcium

scholarly journals Econazole inhibits thapsigargin-induced platelet calcium influx by mechanisms other than cytochrome P-450 inhibition

1993 ◽  
Vol 295 (2) ◽  
pp. 525-529 ◽  
Author(s):  
J G Vostal ◽  
J C Fratantoni
Keyword(s):  
Plasma Membrane ◽  
Antifungal Agents ◽  
Calcium Influx ◽  
Calcium Stores ◽  
Alternative Mechanism ◽  
Resting Cells ◽  
Calcium Efflux ◽  
Plasma Membrane Permeability ◽  
Cytochrome P 450 ◽  
Internal Calcium

Cytochrome P-450 has been suggested as a mediator of the signal between depleted platelet calcium stores and an increase in plasma membrane permeability to calcium which follows depletion of the stores. This hypothesis is based on the observations that inhibitors of cytochrome P-450, such as the imidazole antifungal agents, also inhibit influx of a calcium surrogate (manganese) into calcium-depleted platelets. We tested the effects of econazole and of a cytochrome P-450 inhibitor, carbon monoxide (CO), on thapsigargin (TG)-induced platelet 45Ca2+ influx. TG specifically depletes internal calcium stores and activates store-regulated calcium influx. Econazole blocked 45Ca2+ influx when it was added before TG (IC50 11 microM). Econazole at a concentration (20 microM) that inhibited 83% of TG-induced calcium influx was not inhibitory to TG-induced calcium efflux from 45Ca(2+)-loaded platelets, and did not affect calcium fluxes in resting platelets. This econazole concentration was also inhibitory to calcium influx even when it was added after the stores had been calcium-depleted by EGTA and TG for 15 min and the signal to increase calcium influx had already been generated. Inhibition of cytochrome P-450 with CO bubbled through platelet suspensions did not change calcium influx in resting cells and potentiated TG-induced calcium influx (160% of control calcium accumulation at 20 min). This effect appeared to be concentration-dependent, such that a 5 min exposure to CO produced a greater influx potentiation than a 3 min exposure. These observations indicate that (1) cytochrome P-450 does not mediate store-regulated calcium influx, and (2) econazole probably inhibits store-regulated calcium influx by an alternative mechanism, such as interaction with plasma membrane calcium channels.

ATP regulates calcium leak from agonist‐sensitive internal calcium stores

1996 ◽  
Vol 10 (2) ◽  
pp. 302-308 ◽  
Author(s):  
Aldebaran M. Hofer ◽  
Silvana Curci ◽  
Terry E. Machen ◽  
Irene Schulz
Keyword(s):  
Calcium Stores ◽  
Internal Calcium

scholarly journals The Role of Protein Kinase A in the Ethanol-Induced Increase in Spontaneous GABA Release Onto Cerebellar Purkinje Neurons

2008 ◽  
Vol 100 (6) ◽  
pp. 3417-3428 ◽  
Author(s):  
M. Katherine Kelm ◽  
Hugh E. Criswell ◽  
George R. Breese
Keyword(s):  
Protein Kinase ◽  
Adenylate Cyclase ◽  
Protein Kinase A ◽  
Calcium Release ◽  
Cannabinoid Receptor ◽  
Gaba Release ◽  
Calcium Stores ◽  
Postsynaptic Neuron ◽  
Current Frequency ◽  
Kinase A

Ethanol increases miniature inhibitory postsynaptic current frequency and decreases the paired-pulse ratio, which suggests that ethanol increases both spontaneous and evoked GABA release, respectively. We have shown previously that ethanol increases GABA release at the rat interneuron–Purkinje cell synapse and that this ethanol effect involves calcium release from internal stores; however, further exploration of the mechanism responsible for ethanol-enhanced GABA release was needed. We found that a cannabinoid receptor 1 (CB1) agonist, WIN-55212, and a GABAB receptor agonist, baclofen, decreased baseline spontaneous GABA release and prevented ethanol from increasing spontaneous GABA release. The CB1 receptor and GABAB receptor are Gα i–linked G protein–coupled receptors with common downstream messengers that include adenylate cyclase and protein kinase A (PKA). Adenylate cyclase and PKA antagonists blocked ethanol from increasing spontaneous GABA release, whereas a PKA antagonist limited to the postsynaptic neuron did not block ethanol from increasing spontaneous GABA release. These results suggest that presynaptic PKA plays an essential role in ethanol-enhanced spontaneous GABA release. Similar to ethanol, we found that the mechanism of the cannabinoid-mediated decrease in spontaneous GABA release involves internal calcium stores and PKA. A PKA antagonist decreased baseline spontaneous GABA release. This effect was reduced after incubating the slice with a calcium chelator, BAPTA-AM, but was unaffected when BAPTA was limited to the postsynaptic neuron. This suggests that the PKA antagonist is acting through a presynaptic, calcium-dependent mechanism to decrease spontaneous GABA release. Overall, these results suggest that PKA activation is necessary for ethanol to increase spontaneous GABA release.

Surfactant Releases Internal Calcium Stores in Neutrophils by G Protein-Mediated Pathway

2002 ◽  
Author(s):  
Mark E. Boston ◽  
G. C. Frech ◽  
Enrique Chacon-Cruz ◽  
E. S. Buescher ◽  
David G. Oelberg
Keyword(s):  
G Protein ◽  
Calcium Stores ◽  
Internal Calcium
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