GABAB receptors and G proteins modulate voltage-dependent calcium channels in cultured rat dorsal root ganglion neurons: Relevance to transmitter release and its modulation

1995 ◽  
Vol 26 (1) ◽  
pp. 29-35
Author(s):  
A. C. Dolphin ◽  
A. Menon-Johansson ◽  
V. Campbell ◽  
N. Berrow ◽  
M. I. Sweeney
Keyword(s):  
Dorsal Root Ganglion ◽  
Calcium Channels ◽  
G Proteins ◽  
Transmitter Release ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Gabab Receptors ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels ◽  
Ganglion Neurons

G-proteins are involved in riluzole inhibition of high voltage-activated calcium channels in rat dorsal root ganglion neurons

1997 ◽  
Vol 762 (1-2) ◽  
pp. 235-239 ◽  
Author(s):  
Chao-Sheng Huang ◽  
Jin-Ho Song ◽  
Keiichi Nagata ◽  
Dennis Twombly ◽  
Jay Z Yeh ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Calcium Channels ◽  
G Proteins ◽  
High Voltage ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Ganglion Neurons

scholarly journals Slow sodium conductances of dorsal root ganglion neurons: intraneuronal homogeneity and interneuronal heterogeneity

1994 ◽  
Vol 72 (6) ◽  
pp. 2796-2815 ◽  
Author(s):  
M. A. Rizzo ◽  
J. D. Kocsis ◽  
S. G. Waxman
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Half Time ◽  
Drg Neurons ◽  
Patch Clamp Technique ◽  
Adult Rat ◽  
Voltage Dependent ◽  
Order Of Magnitude ◽  
Ganglion Neurons

1. Voltage-dependent Na+ conductances were studied in small (18-25 microns diam) adult rat dorsal root ganglion (DRG) neurons with the use of the whole cell patch-clamp technique. Na+ currents were also recorded from larger (44-50 microns diam) neurons and compared with those of the small neurons. 2. The predominant Na+ conductance in the small neurons was selective over tetramethylammonium by at least 10-fold and was resistant to 1 microM external tetrodotoxin (TTX). Na+ conductances in many larger DRG neurons were kinetically faster and, in contrast, were blocked by 1 microM TTX. 3. The Na+ conductance in the small neurons was kinetically slow. Activation half-times were voltage dependent and ranged from 2 ms at -20 mV to 0.7 ms at +50 mV. Approximately 50% of the activation half-time was comprised of an initial delay. Inactivation half-times were voltage dependent and ranged from 11 ms at -20 mV to 2 ms at +50 mV. 4. Peak slow Na+ conductances were near maximal with conditioning potentials negative to -120 mV and were significantly reduced or eliminated with conditioning potentials positive to -40 mV. The slow Na+ conductance increased gradually with test potentials extending from -40 to +40 mV. In some cells the conductance could be saturated at +10 mV. Peak conductance/voltage relationships, although stable in a given neuron, revealed marked variability among neurons, spanning > 20- and 50-mV domains for steady-state activation and inactivation (current availability), respectively. 5. Kinetics remained stable within a given neuron over the course of an experiment. However, considerable kinetic variation was exhibited from neuron to neuron, such that the half-times of activation and of inactivation spanned an order of magnitude. In all small neurons studied there appeared to be a singular kinetic component of the current, based on sensitivity to the conditioning potential, voltage dependence of activation, and inactivation half-time. 6. Unique closing properties were exhibited by Na+ channels of the small neurons. Hyperpolarization following a depolarization-induced fully inactivated state resulted in tail currents that appeared to be the consequence of reactivation of the slow Na+ conductance. Tail currents recorded at various times during a fixed level of depolarization revealed that the underlying channels accumulated into a volatile inactivated state over the course of the preceding depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Permeation of Na+ through a delayed rectifier K+ channel in chick dorsal root ganglion neurons.

1994 ◽  
Vol 104 (4) ◽  
pp. 747-771 ◽  
Author(s):  
M J Callahan ◽  
S J Korn
Keyword(s):  
Dorsal Root Ganglion ◽  
Binding Site ◽  
Dorsal Root ◽  
Reversal Potential ◽  
Dorsal Root Ganglion Neurons ◽  
K Channel ◽  
Delayed Rectifier ◽  
Cation Binding Site ◽  
Voltage Dependent ◽  
Ganglion Neurons

In whole-cell patch clamp recordings from chick dorsal root ganglion neurons, removal of intracellular K+ resulted in the appearance of a large, voltage-dependent inward tail current (Icat). Icat was not Ca2+ dependent and was not blocked by Cd2+, but was blocked by Ba2+. The reversal potential for Icat shifted with the Nernst potential for [Na+]. The channel responsible for Icat had a cation permeability sequence of Na+ > Li+ > TMA+ > NMG+ (PX/PNa = 1:0.33:0.1:0) and was impermeable to Cl-. Addition of high intracellular concentrations of K+, Cs+, or Rb+ prevented the occurrence of Icat. Inhibition of Icat by intracellular K+ was voltage dependent, with an IC50 that ranged from 3.0-8.9 mM at membrane potentials between -50 and -110 mV. This voltage-dependent shift in IC50 (e-fold per 52 mV) is consistent with a single cation binding site approximately 50% of the distance into the membrane field. Icat displayed anomolous mole fraction behavior with respect to Na+ and K+; Icat was inhibited by 5 mM extracellular K+ in the presence of 160 mM Na+ and potentiated by equimolar substitution of 80 mM K+ for Na+. The percent inhibition produced by both extracellular and intracellular K+ at 5 mM was identical. Reversal potential measurements revealed that K+ was 65-105 times more permeant than Na+ through the Icat channel. Icat exhibited the same voltage and time dependence of inactivation, the same voltage dependence of activation, and the same macroscopic conductance as the delayed rectifier K+ current in these neurons. We conclude that Icat is a Na+ current that passes through a delayed rectifier K+ channel when intracellular K+ is reduced to below 30 mM. At intracellular K+ concentrations between 1 and 30 mM, PK/PNa remained constant while the conductance at -50 mV varied from 80 to 0% of maximum. These data suggest that the high selectivity of these channels for K+ over Na+ is due to the inability of Na+ to compete with K+ for an intracellular binding site, rather than a barrier that excludes Na+ from entry into the channel or a barrier such as a selectivity filter that prevents Na+ ions from passing through the channel.

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