BACKGROUND: T-type Ca(2+) channels (TCC) are important for pain transmission, 
especially the Ca(V)3.2 subtype. In this study, we examined the effects of 
intrathecal TCC blockers in the L5/6 spinal nerve ligation pain rat model.
METHODS: Under isoflurane anaesthesia, rats received right L5/6 spinal nerve 
ligation and intrathecal catheters (attached to an infusion pump) were sited. 
After surgery, saline, mibefradil, ethosuximide or NiCl2 were given 
intrathecally for seven days. The right hindpaw withdrawal thresholds to von 
Frey hair stimuli and withdrawal latencies to radiant heat were measured before 
and once daily for seven days after surgery. Double immunofluorescence and 
western blotting were used to examine the expression of Ca(V)3.2 in dorsal root 
ganglion (DRG) and spinal cord.
RESULTS: On post-ligation day seven, rats receiving mibefradil, ethosuximide or 
NiCl2 had significant higher median withdrawal thresholds (15.0, 10.2, and 10.9 
g) and latencies (8.0, 7.6 and 7.6 s) than saline-treated rats (1.6 g and 4.3 s, 
respectively). Ca(V)3.2 was expressed in parvalbumin(+), IB4(+), CGRP(+) and 
VR1(+) neurones in DRG and most neurones in spinal dorsal horn. Ca(V)3.2 was 
up-regulated in the right L5/6 DRG and spinal cord seven days after nerve 
ligation.
CONCLUSIONS: In this study, we demonstrated that intrathecal TCC blockers 
attenuate the development of nerve injury-induced mechanical allodynia and 
thermal hyperalgesia. Our data suggest that continuous intrathecal infusion of 
TCC or Ca(V)3.2 blockers may be a promising alternative for the management of 
nerve injury-induced pain.