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 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

Pancreatic polypeptide inhibits calcium channels in rat sympathetic neurons via two signaling pathways

1995 ◽  
Vol 73 (3) ◽  
pp. 1323-1328 ◽  
Author(s):  
L. P. Wollmuth ◽  
M. S. Shapiro ◽  
B. Hille
Keyword(s):  
G Protein ◽  
Pertussis Toxin ◽  
Pancreatic Polypeptide ◽  
Sympathetic Neurons ◽  
Whole Cell ◽  
Adult Rat ◽  
Voltage Dependent ◽  
Cervical Ganglion ◽  
Gamma S ◽  
Ca2 Channels

1. We studied modulation of N-type Ca2+ channels in adult rat superior cervical ganglion (SCG) neurons by pancreatic polypeptide (PP) using whole cell clamp. In large (> 20 pF) SCG neurons, PP inhibited ICa (35 +/- 2%, mean +/- SE) in a concentration-dependent fashion, with one-half maximal inhibition at 19 nM. 2. One-third of the inhibition was blocked by pertussis toxin, about one-half was blocked by N-ethylmaleimide (NEM) treatments, and about one-half was voltage dependent. The NEM-insensitive component of the PP inhibition was voltage independent and not significantly blocked by intracellular Ca2+ chelators. 3. The NEM-insensitive component was only weakly attenuated by GDP-beta-S, and moderately reversible with guanosine 5'-triphosphate (GTP)-gamma-S, in the whole cell pipette, leaving open the possibility that it is not mediated by a G protein. 4. Hence, PP inhibits ICa via two mechanisms: one G-protein-mediated and the other possibly G-protein independent. The former pathway is sensitive to pertussis toxin (PTX) and NEM, voltage dependent, and shared by several other transmitters in these cells. The latter pathway is PTX-and NEM-insensitive, not voltage dependent, and not affected by the presence of intracellular Ca2+ chelators.

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

Modulation of Ca2+ Currents by Various G Protein-Coupled Receptors in Sympathetic Neurons of Male Rat Pelvic Ganglia

1997 ◽  
Vol 78 (2) ◽  
pp. 780-789 ◽  
Author(s):  
Yu Zhu ◽  
Jerrel L. Yakel
Keyword(s):  
G Protein ◽  
Sympathetic Neurons ◽  
Inhibitory Effect ◽  
G Protein Coupled Receptors ◽  
Male Rat ◽  
Tetraacetic Acid ◽  
Patch Clamp Recording ◽  
Major Pelvic Ganglion ◽  
G Protein Coupled ◽  
Pelvic Ganglia

Zhu, Yu and Jerrel L. Yakel. Modulation of Ca2+ currents by various G protein-coupled receptors in sympathetic neurons of male rat pelvic ganglia. J. Neurophysiol. 78: 780–789, 1997. The modulation of voltage-gated calcium (Ca2+) channels by various G protein-coupled receptor pathways was investigated in sympathetic neurons of the male rat major pelvic ganglion (MPG). Standard whole cell patch-clamp recording techniques were used to record Ca2+ currents from acutely dissociated neurons. The activation of muscarinic receptors, which uses a G protein pathway that was not blocked by either pertussis toxin (PTX) or cholera toxin (CTX), inhibited both N-type and L-type Ca2+ channels. The activation of α2 noradrenergic receptors with the selective agonist UK14304, which used primarily a PTX-sensitive G protein pathway, inhibited only N-type Ca2+ channels. The activation ofvasoactive intestinal polypeptide (VIP) receptors, which used a CTX-sensitive G protein pathway, also inhibited only N-type Ca2+ channels. UK14304 and VIP induced a bell-shaped inhibition of the Ca2+ current with a peak inhibition at around +10 mV and decreasing inhibition at more positive potentials. In contrast, the muscarine-induced Ca2+ current inhibition was not bell shaped and was more prominent at more positive potentials. Furthermore, a large depolarization, which relieved the current inhibition by UK14304 and VIP, did not relieve the inhibition by muscarine. Besides inhibiting the Ca2+ current, UK14304 and VIP also slowed the activation kinetics, an effect not seen with muscarine. Replacing external Ca2+ with Ba2+ and replacing internal ethylene glycol-bis(β-aminoethyl ether)- N,N,N′,N′-tetraacetic acid (EGTA) with high bis-( o-aminophenoxy)- N,N,N′,N′-tetraacetic acid (BAPTA) completely blocked the inhibitory effect of muscarine. However, the inhibitory effects of both UK14304 and VIP were unaffected under these conditions. Surprisingly, the facilitation of the Ca2+ current was eliminated under these strong calcium-buffering conditions. The activation of protein kinase C (PKC) with phorbol 12-myristate 13-acetate (PMA) increases the amplitude of the Ca2+ current, diminishes facilitation, and reduces the inhibition of this current by UK14304 and VIP. However, PKC activation did not reduce the muscarine-induced Ca2+ current inhibition. In summary, our data suggest that muscarine uses a mechanism different from UK14304 and VIP to modulate the N-type Ca2+ channels in sympathetic neurons of the MPG. Although VIP and UK14304 use different G protein pathways, these two different pathways most likely converge downstream to compete for the same target site on the N-type Ca2+ channels.

Control of voltage‐dependent Ca 2+ channels by G protein‐coupled receptors

1988 ◽  
Vol 2 (12) ◽  
pp. 2784-2790 ◽  
Author(s):  
Walter Rosenthal ◽  
Jürgen Hescheler ◽  
Wolfgang Trautwein ◽  
Günter Schultz
Keyword(s):  
G Protein ◽  
G Protein Coupled Receptors ◽  
Voltage Dependent ◽  
G Protein Coupled

scholarly journals Calcineurin Modulates G Protein-Mediated Inhibition of N-Type Calcium Channels in Rat Sympathetic Neurons

1997 ◽  
Vol 78 (2) ◽  
pp. 1161-1169 ◽  
Author(s):  
Yu Zhu ◽  
Jerrel L. Yakel
Keyword(s):  
Calcium Channels ◽  
G Protein ◽  
Sympathetic Neurons ◽  
Somatostatin Receptor ◽  
Male Rat ◽  
Patch Clamp Recording ◽  
Whole Cell Patch Clamp ◽  
Major Pelvic Ganglion ◽  
G Protein Coupled ◽  
Kinetics Of

Zhu, Yu and Jerrel L. Yakel. Calcineurin modulates G protein-mediated inhibition of N-type calcium channels in rat sympathetic neurons. J. Neurophysiol. 78: 1161–1169, 1997. The modulation of N-type voltage-gated calcium (Ca2+) channels by G protein-coupled receptors was investigated in sympathetic neurons of the male rat major pelvic ganglion (MPG) with the use of whole cell patch-clamp recording techniques from acutely dissociated neurons. By inhibiting calcineurin, a Ca2+/calmodulin-regulatedprotein phosphatase, the α2 noradrenergic and somatostatin receptor-induced inhibition of these N-type Ca2+ channels was greatly reduced. Both of these receptor pathways utilize a pertussis toxin-sensitive G protein (GPTX). The guanosine 5′-o-(3-thiotriphosphate) (GTPγS)-induced decrease in the amplitude and activation kinetics of Ca2+ currents, an effect that was similar to the activation of GPTX-coupled receptors, also was reduced by the inhibition of calcineurin. Calcineurin does not regulate the muscarinic receptor-induced inhibition of the N-type Ca2+ channels, a pathway that utilizes a different G protein in the MPG neurons. Thus calcineurin appears to selectively regulate the coupling between the GPTX and the Ca2+ channel.

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