scholarly journals Estradiol attenuates the adenosine triphosphate-induced increase of intracellular calcium through group II metabotropic glutamate receptors in rat dorsal root ganglion neurons

2011 ◽  
Vol 89 (11) ◽  
pp. 1707-1710 ◽  
Author(s):  
Victor Chaban ◽  
Jichang Li ◽  
John S. McDonald ◽  
Andrea Rapkin ◽  
Paul Micevych
Keyword(s):  
Dorsal Root Ganglion ◽  
Intracellular Calcium ◽  
Glutamate Receptors ◽  
Adenosine Triphosphate ◽  
Dorsal Root ◽  
Metabotropic Glutamate Receptors ◽  
Dorsal Root Ganglion Neurons ◽  
Metabotropic Glutamate ◽  
Group Ii ◽  
Ganglion Neurons

Activation of Ca2+-Dependent Currents in Dorsal Root Ganglion Neurons by Metabotropic Glutamate Receptors and Cyclic ADP-Ribose Precursors

1997 ◽  
Vol 77 (5) ◽  
pp. 2573-2584 ◽  
Author(s):  
Jane H. Crawford ◽  
John F. Wootton ◽  
Guy R. Seabrook ◽  
Roderick H. Scott
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate Receptor ◽  
Receptor Activation ◽  
Dorsal Root Ganglion Neurons ◽  
Metabotropic Glutamate ◽  
Intracellular Ca ◽  
Inward Currents ◽  
Ganglion Neurons

Crawford, Jane H., John F. Wootton, Guy R. Seabrook, and Roderick H. Scott. Activation of Ca2+-dependent currents in dorsal root ganglion neurons by metabotropic glutamate receptors and cyclic ADP-ribose precursors. J. Neurophysiol. 77: 2573–2584, 1997. Cultured dorsal root ganglion neurons were voltage clamped at −90 mV to study the effects of intracellular application of nicotinamide adenine dinucleotide (βNAD+), intracellular flash photolysis of caged 3′,5′-cyclic guanosine monophosphate (cGMP), and metabotropic glutamate receptor activation. The activation of metabotropic glutamate receptors evoked inward Ca2+-dependent currents in most cells. This was mimicked both by intracellular flash photolysis of the caged axial isomer of cGMP [P-1-(2-nitrophenyl)ethyl cGMP] and intracellular application of βNAD+. Whole cell Ca2+-activated inward currents were used as a physiological index of raised intracellular Ca2+ levels. Extracellular application of 10 μM glutamate evoked the activation of Ca2+-dependent inward currents, thus reflecting a rise in intracellular Ca2+ levels. Similar inward currents were also activated after isolation of metabotropic glutamate receptor activation by application of 10 μM glutamate in the presence of 20 μM 6-cyano-7-nitroquinoxaline-2,3-dione and 20 μM dizocilpine maleate (MK 801), or by extracellular application of 10 μM trans-(1 S,3 R)-1-amino-1,3-cyclopentanedicarboxylic acid. Intracellular photorelease of cGMP, from its caged axial isomer, in the presence of βNAD+ was also able to evoke similar Ca2+-dependent inward currents. Intracellular application of βNAD+ alone produced a concentration-dependent effect on inward current activity. Responses to both metabotropic glutamate receptor activation and cGMP were suppressed by intracellular ryanodine, chelation of intracellular Ca2+ by bis-( o-aminophenoxy)- N,N,N′,N′-tetraacetic acid, and depletion of intracellular Ca2+ stores, but were insensitive to the removal of extracellular Ca2+. Therefore both cGMP, possibly via a mechanism that involves βNAD+ and/or cyclic ADP-ribose, and glutamate can mobilize intracellular Ca2+ from ryanodine-sensitive stores in sensory neurons.

scholarly journals Role of CaMK II α in the Injury of Dorsal Root Ganglion Neurons Induced by Ropivacaine Hydrochloride in the Dorsal Root Ganglion of Rats

2021 ◽  
pp. 1-7
Author(s):  
Wu Zhaoxia ◽  
Chen Meixin ◽  
Li Yiqun ◽  
Yang Shuxuan ◽  
Wen Xianjie
Keyword(s):  
Dorsal Root Ganglion ◽  
Cell Viability ◽  
Intracellular Calcium ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Drg Neurons ◽  
Apoptosis Rate ◽  
Ganglion Neurons ◽  
Ropivacaine Hydrochloride

Objective: To investigate whether CaMKⅡα participates in the dorsal root ganglion neurotoxicity induced by ropivacaine hydrochloride. Methods: DRG neurons were isolated from 1-day-old SD rats and cultured in vitro. pAd-shRNA-CaMKⅡα-DRG cells were constructed by RNA interference technique to inhibit the expression of CaMKⅡα. The experiment was divided into six groups: DRG group (DRG group), vector DRG group (vector group), pAd-shRNA- CaMKIIα-DRG group (pAd-shRNA group), DRG + ropivacaine group (DRG + R group), vector DRG + ropivacaine group (vector + R group), pAd-shRNA-CaMKII α - DRG + ropivacaine group (pAd-shRNA + R group), and the last three groups were treated with 3 mM ropivacaine hydrochloride for 4 hours. MTT assay was used to detect cell viability, flow cytometry was used to detect cell apoptosis rate, laser confocal microscopy was used to detect intracellular calcium level, and real-time PCR was used to detect the mRNA expression of CaMKⅡα, Cav3.2 and Cav3.3. Results: The cell viability of DRG+R group, vector+R group and pAd-shRNA+R group decreased significantly after 3 mM ropivacaine hydrochloride treatment for 4 h. Compared with DRG+R group, the cell viability of pAd-shRNA+R group was significantly higher. After 3 mM ropivacaine hydrochloride treatment for 4 h, the apoptosis rate of DRG + R group, vector + R group and pAd-shRNA + R group increased significantly. Compared with DRG+R group, the apoptosis rate in pAd shRNA+R group was significantly lower. After 3 mM ropivacaine hydrochloride treatment for 4 h, the intracellular calcium levels in DRG + R group, vector + R group and pAd-shRNA + R group were significantly increased, and the intracellular calcium levels in pAd-shRNA + R group were significantly lower than those in DRG + R group. The mRNA expressions of CaMKⅡα, Cav3.2 and Cav3.3 were significantly decreased in pAd- shRNA group. The mRNA expressions of CaMK Ⅱ α, Cav3.2 and Cav3.3 were up-regulated in DRG + R group, vector + R group and pAd-shRNA + R group after 3 mm ropivacaine treatment for 4 h. The mRNA expressions of CaMKⅡα, Cav3.2 and Cav3.3 in pAd-shRNA + R group were significantly lower than those in DRG + R group. Conclusion: Inhibition of CaMKⅡα expression can down regulate the expression of Cav3.2 and Cav3.3 mRNA, increase cell viability of DRG neurons, reduce the apoptosis rate, and improve the dorsal root ganglion neurotoxicity induced by ropivacaine hydrochloride.

scholarly journals Reply to “TRPA1-dependent calcium transients and CGRP release in DRG neurons require extracellular calcium”

2020 ◽  
Vol 219 (6) ◽  
Author(s):  
Bing Liu ◽  
Muhammad Younus ◽  
Suhua Sun ◽  
Yiman Li ◽  
Yuan Wang ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Intracellular Calcium ◽  
Dorsal Root ◽  
Extracellular Calcium ◽  
Dorsal Root Ganglion Neurons ◽  
Calcium Transients ◽  
Drg Neurons ◽  
Cgrp Release ◽  
Ganglion Neurons

In this issue, Gebhardt et al. (2020. J. Cell Biol.https://doi.org/10.1083/jcb.201702151) express interest in our recently published work (Shang et al. 2016. J. Cell Biol.https://doi.org/10.1083/jcb.201603081). Here, we would like to address their concerns regarding the lysosomal TRPA1-mediated intracellular calcium transients in dorsal root ganglion neurons.

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