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The Journal of Neurophysiology Vol. 83 No. 4 April 2000, pp. 2227-2238
Copyright ©2000 by the American Physiological Society
Department of Neurology, Yale University School of Medicine, New Haven 06510; and Department of Veterans Affairs, Neuroscience Research Center, West Haven, Connecticut 06516
Baccei, Mark L. and
Jeffery D. Kocsis.
Voltage-Gated Calcium Currents in Axotomized Adult Rat Cutaneous
Afferent Neurons. J. Neurophysiol. 83: 2227-2238, 2000. The effect of sciatic nerve injury on the
somatic expression of voltage-gated calcium currents in adult rat
cutaneous afferent dorsal root ganglion (DRG) neurons identified via
retrograde Fluoro-gold labeling was studied using whole cell
patch-clamp techniques. Two weeks after a unilateral ligation and
transection of the sciatic nerve, the L4-L5
DRG were dissociated and barium currents were recorded from cells 3-10
h later. Cutaneous afferents (35-50 µm diam) were classified as type
1 (possessing only high-voltage-activated currents; HVA) or type 2 (having both high- and low-voltage-activated currents). Axotomy did
not change the percentage of neurons exhibiting a type 2 phenotype or
the properties of low-threshold T-type current found in type 2 neurons.
However, in type 1 neurons the peak density of HVA current available at
a holding potential of 
60 mV was reduced in axotomized neurons
(83.9 ± 5.6 pA/pF, n = 53) as compared with
control cells (108.7 ± 6.9 pA/pF, n = 58, P < 0.01, unpaired t-test). A
similar reduction was observed at more negative holding potentials,
suggesting differences in steady-state inactivation are not responsible
for the effect. Separation of the type 1 cells into different size
classes indicates that the reduction in voltage-gated barium current
occurs selectively in the larger (capacitance >80 pF) cutaneous
afferents (control: 112.4 ± 10.6 pA/pF, n = 30; ligated: 72.6 ± 5.0 pA/pF, n = 36;
P < 0.001); no change was observed in cells with
capacitances of 45-80 pF. Isolation of the N- and P\Q-type components of the HVA current in the large
neurons using 
-conotoxin GVIA and -agatoxin TK suggests a
selective reduction in N-type barium current after nerve injury, as the
density of -CgTx GVIA-sensitive current decreased from 56.9 ± 6.6 pA/pF in control cells (n = 13) to 31.3 ± 4.6 pA/pF in the ligated group (n = 12;
P < 0.005). The HVA barium current of large
cutaneous afferents also demonstrates a depolarizing shift in the
voltage dependence of inactivation after axotomy. Injured type 1 cells exhibited faster inactivation kinetics than control neurons, although the rate of recovery from inactivation was similar in the two groups.
The present results indicate that nerve injury leads to a
reorganization of the HVA calcium current properties in a subset of
cutaneous afferent neurons.
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