Changes in expression of two tetrodotoxin-resistant sodium channels and their currents in dorsal root ganglion neurons after sciatic nerve injury butnot rhizotomy
Aa. Sleeper et al., Changes in expression of two tetrodotoxin-resistant sodium channels and their currents in dorsal root ganglion neurons after sciatic nerve injury butnot rhizotomy, J NEUROSC, 20(19), 2000, pp. 7279-7289
Two TTX-resistant sodium channels, SNS and NaN, are preferentially expresse
d in c-type dorsal root ganglion (DRG) neurons and have been shown recently
to have distinct electrophysiological signatures, SNS producing a slowly i
nactivating and NaN producing a persistent sodium current with a relatively
hyperpolarized voltage-dependence. An attenuation of SNS and NaN transcrip
ts has been demonstrated in small DRG neurons after transection of the scia
tic nerve. However, it is not known whether changes in the currents associa
ted with SNS and NaN or in the expression of SNS and NaN channel protein oc
cur after axotomy of the peripheral projections of DRG neurons or whether s
imilar changes occur after transection of the central (dorsal root) project
ions of DRG neurons.
Peripheral and central projections of L4/5 DRG neurons in adult rats were a
xotomized by transection of the sciatic nerve and the L4 and L5 dorsal root
s, respectively. DRG neurons were examined using immunocytochemical and pat
ch-clamp methods 9-12 d after sciatic nerve or dorsal root lesion. Levels o
f SNS and NaN protein in the two types of injuries were paralleled by their
respective TTX-resistant currents. There was a significant decrease in SNS
and NaN signal intensity in small DRG neurons after peripheral, but not ce
ntral, axotomy compared with control neurons. Likewise, there was a signifi
cant reduction in slowly inactivating and persistent TTX-resistant currents
in these neurons after peripheral, but not central, axotomy compared with
control neurons. These results indicate that peripheral, but not central, a
xotomy results in a reduction in expression of functional SNS and NaN chann
els in c-type DRG neurons and suggest a basis for the altered electrical pr
operties that are observed after peripheral nerve injury.