scholarly journals Modulation of Voltage-Gated Ca2+ Channels by G Protein-Coupled Receptors in Celiac-Mesenteric Ganglion Neurons of Septic Rats

PLoS ONE ◽  
2015 ◽  
Vol 10 (5) ◽  
pp. e0125566 ◽  
Author(s):  
Mohamed Farrag ◽  
Lacee J. Laufenberg ◽  
Jennifer L. Steiner ◽  
Gregory E. Weller ◽  
Charles H. Lang ◽  
...  
Keyword(s):  
G Protein ◽  
G Protein Coupled Receptors ◽  
Voltage Gated ◽  
Mesenteric Ganglion ◽  
Ganglion Neurons ◽  
G Protein Coupled ◽  
Ca2 Channels

scholarly journals N-Arachidonoyl l-Serine, a Putative Endocannabinoid, Alters the Activation of N-Type Ca2+ Channels in Sympathetic Neurons

2008 ◽  
Vol 100 (2) ◽  
pp. 1147-1151 ◽  
Author(s):  
Juan Guo ◽  
Damian J. Williams ◽  
Stephen R. Ikeda
Keyword(s):  
G Protein ◽  
Sympathetic Neurons ◽  
G Protein Coupled Receptors ◽  
Whole Cell Patch Clamp ◽  
Voltage Dependent ◽  
Nervous System Function ◽  
Ganglion Neurons ◽  
G Protein Coupled ◽  
Hyperpolarizing Shift ◽  
Ca2 Channels

The effect of N-arachidonoyl l-serine (ARA-S), a recently discovered lipoamino acid found in the CNS, on N-type Ca2+ channels of rat sympathetic ganglion neurons was determined using whole cell patch clamp. Application of ARA-S produced a rapid and reversible augmentation of Ca2+ current that was voltage dependent and resulted from a hyperpolarizing shift in the activation curve. ARA-S did not influence G protein modulation of Ca2+ channels and appeared to act independently of G-protein-coupled receptors. These findings provide a foundation for investigating possible roles for ARA-S in nervous system function.

scholarly journals Disabling Gβγ SNARE interaction in transgenic mice disrupts GPCR-mediated presynaptic inhibition leading to physiological and behavioral phenotypes

2018 ◽  
Author(s):  
Zack Zurawski ◽  
Analisa D. Thompson Gray ◽  
Lillian J. Brady ◽  
Brian Page ◽  
Emily Church ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Calcium Channels ◽  
G Protein ◽  
Presynaptic Inhibition ◽  
Receptor Activation ◽  
G Protein Coupled Receptors ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Crucial Component ◽  
G Protein Coupled

ABSTRACTGi/o-coupled G-protein coupled receptors modulate neurotransmission presynaptically through inhibition of exocytosis. Release of Gβγ subunits decreases the activity of voltage-gated calcium channels (VGCC), decreasing excitability. A less understood Gβγ–mediated mechanism downstream of calcium entry is the binding of Gβγ to SNARE complexes. Here, we create a mouse partially deficient in this interaction. SNAP25Δ3 homozygote animals are developmentally normalbut impaired gait and supraspinal nociception. They also have elevated stress-induced hyperthermia and impaired inhibitory postsynaptic responses to α2A-AR, but normal inhibitory postsynaptic responses to Gi/o-coupled GABAB receptor activation. SNAP25Δ3 homozygotes have deficits in inhibition of hippocampal postsynaptic responses to 5 HT1b agonists that affect hippocampal learning. These data suggest that Gi/o-coupled GPCR inhibition of exocytosis through the Gβγ-SNARE interaction is a crucial component of numerous physiological and behavioral processes.

Inhibition of Dendritic Calcium Influx by Activation of G-Protein–Coupled Receptors in the Hippocampus

1997 ◽  
Vol 78 (6) ◽  
pp. 3484-3488 ◽  
Author(s):  
Huanmian Chen ◽  
Nevin A. Lambert
Keyword(s):  
Calcium Channels ◽  
Action Potential ◽  
G Protein ◽  
Pyramidal Neuron ◽  
Action Potentials ◽  
Calcium Influx ◽  
G Protein Coupled Receptors ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
G Protein Coupled

Chen, Huanmian and Nevin A. Lambert. Inhibition of dendritic calcium influx by activation of G-protein–coupled receptors in the hippocampus. J. Neurophysiol. 78: 3484–3488, 1997. Gi proteins inhibit voltage-gated calcium channels and activate inwardly rectifying K+ channels in hippocampal pyramidal neurons. The effect of activation of G-protein–coupled receptors on action potential-evoked calcium influx was examined in pyramidal neuron dendrites with optical and extracellular voltage recording. We tested the hypotheses that 1) activation of these receptors would inhibit calcium channels in dendrites; 2) hyperpolarization resulting from K+ channel activation would deinactivate low-threshold, T-type calcium channels on dendrites, increasing calcium influx mediated by these channels; and 3) activation of these receptors would inhibit propagation of action potentials into dendrites, and thus indirectly decrease calcium influx. Activation of adenosine receptors, which couple to Gi proteins, inhibited calcium influx in cell bodies and proximal dendrites without inhibiting action-potential propagation into the proximal dendrites. Inhibition of dendritic calcium influx was not changed in the presence of 50 μM nickel, which preferentially blocks T-type channels, suggesting influx through these channels is not increased by activation of G-proteins. Adenosine inhibited propagation of action potentials into the distal branches of pyramidal neuron dendrites, leading to a three- to fourfold greater inhibition of calcium influx in the distal dendrites than in the soma or proximal dendrites. These results suggest that voltage-gated calcium channels are inhibited in pyramidal neuron dendrites, as they are in cell bodies and terminals and thatG-protein–mediated inhibition of action-potential propagation can contribute substantially to inhibition of dendritic calcium influx.

scholarly journals Structural and Functional Characteristics of TRP Ca2+ channels activated by G-protein-coupled Receptors

1998 ◽  
Vol 76 ◽  
pp. 93
Author(s):  
Takaharu Qkada ◽  
Shunichi Shimizu ◽  
Minoru Wakamori ◽  
Naoyuki Takada ◽  
Akito Maeda ◽  
...  
Keyword(s):  
G Protein ◽  
G Protein Coupled Receptors ◽  
Functional Characteristics ◽  
G Protein Coupled ◽  
Ca2 Channels

scholarly journals Gα14 subunit-mediated inhibition of voltage-gated Ca2+ and K+ channels via neurokinin-1 receptors in rat celiac-superior mesenteric ganglion neurons

2016 ◽  
Vol 115 (3) ◽  
pp. 1577-1586
Author(s):  
Shigekazu Sugino ◽  
Mohamed Farrag ◽  
Victor Ruiz-Velasco
Keyword(s):  
Small Interference Rna ◽  
Voltage Gated ◽  
M Current ◽  
Mesenteric Ganglion ◽  
Voltage Dependent ◽  
Current Block ◽  
Neurokinin 1 ◽  
Ganglion Neurons ◽  
G Protein Coupled ◽  
Channel Currents

The mechanisms by which G proteins modulate voltage-gated Ca2+ channel currents (CaV), particularly CaV2.2 and CaV2.3, are voltage dependent (VD) or voltage independent (VI). VD pathways are typically mediated by Gαi/o and GαS subfamilies. On the other hand, VI inhibition modulation is coupled to the Gαq subfamily and signaling pathways downstream of phospholipase C stimulation. In most studies, this latter pathway has been shown to be linked to Gαq and/or Gα11 protein subunits. However, there are no studies that have examined whether natively expressed Gα14 subunits (Gαq subfamily member) couple G protein-coupled receptors (GPCR) with CaV2.2 channels. We report that Gα14 subunits functionally couple the substance P (SP)/neurokinin-1 (NK-1) receptor pathway to CaV2.2 channels in acutely dissociated rat celiac-superior mesenteric ganglion (CSMG) neurons. Exposure of CSMG neurons to SP blocked the CaV2.2 currents in a predominantly VD manner that was pertussis toxin and cholera toxin resistant, as well as Gαq/11 independent. However, silencing Gα14 subunits significantly attenuated the SP-mediated Ca2+ current block. In another set of experiments, exposure of CSMG neurons to SP led to the inhibition of KCNQ K+ M-currents. The SP-mediated M-current block was significantly reduced in neurons transfected with Gα14 small-interference RNA. Finally, overexpression of the GTP-bound Gαq/11 binding protein RGS2 did not alter the block of M-currents by SP but significantly abolished the oxotremorine methiodide-mediated M-current inhibition. Taken together, these results provide evidence of a new Gα14-coupled signaling pathway that modulates CaV2.2 and M-currents via SP-stimulated NK-1 receptors in CSMG neurons.

scholarly journals An advance about the genetic causes of epilepsy

2021 ◽  
Vol 271 ◽  
pp. 03068
Author(s):  
Yu Sun ◽  
Licheng Lu ◽  
Lanxin Li ◽  
Jingbo Wang
Keyword(s):  
G Protein ◽  
Gaba Receptors ◽  
Glucose Transporter ◽  
Transmembrane Proteins ◽  
G Protein Coupled Receptors ◽  
Genetic Defects ◽  
Voltage Gated ◽  
Voltage Gated Channels ◽  
G Protein Coupled ◽  
Mutant Genes

Human hereditary epilepsy has been found related to ion channel mutations in voltage-gated channels (Na+, K+, Ca2+, Cl-), ligand gated channels (GABA receptors), and G-protein coupled receptors, such as Mass1. In addition, some transmembrane proteins or receptor genes, including PRRT2 and nAChR, and glucose transporter genes, such as GLUT1 and SLC2A1, are also about the onset of epilepsy. The discovery of these genetic defects has contributed greatly to our understanding of the pathology of epilepsy. This review focuses on introducing and summarizing epilepsy-associated genes and related findings in recent decades, pointing out related mutant genes that need to be further studied in the future.

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