Changes in the ionic mechanisms of electrical excitability in the somatic membrane of rat dorsal root ganglion neurons during ontogenesis. Correlations between inward current densities

1987 ◽  
Vol 18 (6) ◽  
pp. 581-586
Author(s):  
S. A. Fedulova ◽  
P. G. Kostyuk ◽  
N. S. Veselovskii
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Electrical Excitability ◽  
Somatic Membrane ◽  
Inward Current ◽  
Ionic Mechanisms ◽  
Current Densities ◽  
Ganglion Neurons

Inhibition of a Hyperpolarization-Activated Current by Clonidine in Rat Dorsal Root Ganglion Neurons

1998 ◽  
Vol 80 (3) ◽  
pp. 1094-1104 ◽  
Author(s):  
Junichi Yagi ◽  
Rhyuji Sumino
Keyword(s):  
Dorsal Root Ganglion ◽  
Current Pulse ◽  
Dorsal Root ◽  
Reversal Potential ◽  
Dorsal Root Ganglion Neurons ◽  
Drg Neurons ◽  
Current Clamp ◽  
Inward Current ◽  
Hyperpolarization Activated Current ◽  
Ganglion Neurons

Yagi, Junichi and Rhyuji Sumino. Inhibition of a hyperpolarization-activated current by clonidine in rat dorsal root ganglion neurons. J. Neurophysiol. 80: 1094–1104, 1998. Whole cell voltage- and current-clamp recordings were carried out to investigate the effects of clonidine, an α2-adrenoceptor agonist, in L4 and L5 dorsal root ganglion (DRG) neurons of the rat. In voltage-clamp mode, application of 20 μM clonidine reversibly reduced the inward current evoked by hyperpolarizing voltage steps. The “clonidine-sensitive current” was obtained by subtracting the current during clonidine application from the control current, and its properties were as follows. 1) It was a slowly activating inward current evoked by hyperpolarization. 2) The reversal potential in the standard extracellular solution ([K+]o = 5 mM, [Na+]o = 151 mM) was −38.3 mV, and reduction of [Na+]o shifted it to a more negative potential, whereas an increase of [K+]o shifted it to a more positive potential, indicating that the current was carried by Na+ and K+ ( P Na/ P K = 0.22). 3) The relationship between the chord conductance underlying the clonidine-sensitive current and voltage could be fitted by a Boltzmann equation. These results indicate that the clonidine-sensitive current corresponds to a hyperpolarization-activated current ( I h), i.e., clonidine inhibits I h in rat DRG neurons. DRG neurons were classified as small (15.9–32.9 μm diam), medium-sized (33–42.9 μm), and large (43–63.6 μm), and 7 of 19, 24 of 25, and 22 of 22 of these types exhibited I h with mean ± SE clonidine-induced inhibition values of 36.1 ± 3.5% ( n = 7), 43.1 ± 3.7% ( n = 24), and 35.1 ± 2.7% ( n = 22), respectively. Clonidine application to L4 and L5 DRG neurons excised from rats the sciatic nerves of which had been transected 14–35 days previously (transected DRG neurons) also reduced I h. In current-clamp mode, 9 of 13 intact and 4 of 6 transected medium-sized DRG neurons that exhibited I h responded to clonidine with hyperpolarization (>2 mV). Some medium-sized DRG neurons exhibited repetitive action potentials in response to a depolarizing current pulse, and clonidine reduced the firing discharge frequencies in 8 of 11 intact and 3 of 4 transected neurons tested. Injection of a hyperpolarizing current pulse produced time-dependent rectification in DRG neurons that exhibited I h, and clonidine blocked this rectification in all intact and transected neurons tested. These results suggest that inhibition of I h due to α2-adrenoceptor activation contributes to modulation of DRG neuronal activity in rats. On the basis of our findings, we discuss the possible mechanisms whereby sympathetically released norepinephrine modulates the abnormal activity of DRG neuronal cell bodies after nerve injury.

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