Jl. Zhou et al., Development of purinergic sensitivity in sensory neurons after peripheral nerve injury in the rat, BRAIN RES, 915(2), 2001, pp. 161-169
Purinoceptors are present in the cell bodies as well as in both peripheral
and central terminals of many sensory neurons, where they may play a role i
n sensory transmission, including pain. After peripheral nerve injury at th
e spinal nerve level, some axotomized afferent neurons develop ongoing disc
harges (ectopic discharges) that originate in the dorsal root ganglion (DRG
). In the present study, we attempted to determine whether or not purinergi
c sensitivity develops in injured sensory neurons which display ectopic dis
charges, as well as in silent units. The L-4 and L-5 spinal nerves were lig
ated in Sprague-Dawley rats. Four to 21 days after the surgery, the DRGs wi
th attached dorsal roots and spinal nerves were removed and ectopic dischar
ges were recorded from teased dorsal root fascicles using an in vitro recor
ding set-up. The results showed that 75.6 and 65.1% of the chronically axot
omized DRG neurons displaying ectopic discharges enhanced their activity af
ter application of adenosine 5'-triphosphate (ATP, I mM) or alpha,beta -met
hylene ATP (mATP, 100 muM), respectively. In addition, application of these
purinoceptor agonists evoked activity in 7 of 28 axotomized DRG neurons, w
hich did not show ongoing discharges. In contrast, only I of 34 DRG neurons
acutely isolated from normal rats (no previous spinal nerve ligation) resp
onded to either mATP or ATR In most of the tested units. mATP-induced enhan
cement of ectopic discharges was blocked by non-specific P2X receptor antag
onists, PPADS or suramin. The data from the present study suggest that puri
nergic sensitivity develops in DRG neurons after chronic axotomy and that t
his purinergic sensitivity is likely to be mediated by P2X purinoceptors. T
his acquired purinergic sensitivity may play an important functional role i
n the enhancement of ectopic discharges and exacerbation of pain upon sympa
thetic activation in the neuropathic pain state. (C) 2001 Elsevier Science
BY All rights reserved.