The present study aimed to systematically observe the change of vanilloidreceptor1 (VR1) during in

The present study was conducted to evaluate the characteristics of electroacupuncture (EA)-induced analgesia in mice. Three inbred strains of mice (DBA/2, C57BL/6J, BALB/c) and three outbred strains (ICR, LACA, NIH) were used in the experiment. Two pairs of metallic needles were inserted into acupoints ST 36 and SP 6 connected to an electric pulse generator. EA parameters were set as constant current output with alteration of a positive and negative square wave, 0.6ms in pulse width for 2Hz and 0.3ms for 100Hz. Tail-flick latencies evoked by radiant heat were measured before, during and after EA stimulation. We found that (1) DBA/2 mice showed a significantly more potent analgesic effect than the other five strains in response to both 100 and 2Hz EA. In this case, the intensities were 1.0-2.0-2.0mA, 10 min for each intensity totally 30min. (2) EA analgesia increased as the intensity of stimulation increased from 0.5 to 21 2.0mA, but it remained at this plateau when the intensity further increased from 2.0 to 3.0mA. (3) 10.0mg?kg naloxone was needed to 21 block the analgesic effect induced by 2Hz EA of 2.0mA, but to block that by 100Hz, 25.0mg?kg was necessary. (4) A positive 21 correlation was observed between analgesia induced by morphine at the dose of 5.0mg?kg and by 100Hz EA in two tested strains DBA/2 and C57BL/6J. In conclusion, EA induces reliable, strain-dependent analgesia in mice. The naloxone-reversibility of EA, a measure of whether it is opioid or non-opioid mediated, is dependent upon intensity and frequency.

The protective effects of adenovirus-mediated glia cell linederived neurotrophic factor (GDNF) gene transaction was investigated on cultured motoneurons. First, the dose

Mu-opioid agonists and N-methyl-d-aspartate (NMDA) receptor antagonists have been shown to attenuate mechanical allodynia in neuropathic pain models. We have previously reported that 2Hz ectroacupuncture (EA) produced analgesia via releasing endogenous opioid peptides (i.e.-endorphin and endomorphin) and the activated-opioid receptors. The present study aimed to examine whether ketamine, an NMDAreceptor antagonist, can enhance the anti-allodynic effects induced by 2 HzEAin a rat model of neuropathic pain following spinal nerve ligation (SNL). The results are as follows: (1) EA itself or i.p. injection of ketamine reduced mechanical allodynia (i.e.increase in withdrawal threshold). (2) Although injection of ketamine at a low dose (1.0mg/kg) alone did not influence mechanical withdrawal threshold, combination of ketamine at this dose with EA produced more potent anti-allodynic effect than that induced by EA alone. (3) The anti-allodynic effect of EA combined with ketamine could be reversed by i.p. injection of naloxone (2.0mg/kg). These results suggested that ketamine potentiate the anti-allodynic of EA in rats with spinal nerve ligation, and endogenous opioid system is likely to be involved in this process.

Our previous studies have shown that 100Hz electroacupuncture (EA) produced antinociception through the release of endogenous opioids (mainly dynorphin) and the activated -opioid receptors in normal rats. Acupuncture is an effective treatment in relieving pain, but it develops tolerance after epeated administration. It has been reported that N-methyl-d-aspartate (NMDA) receptor antagonists could increase the antinociceptive effects induced by morphine and delay the development of tolerance to morphine but nothing has yet been described to reduce EA tolerance. Here we test whether ketamine, a non-competitive NMDA receptor antagonist, would enhance 100Hz EA antinociception as well as prevent or delay the development of chronic tolerance to 100Hz EA in normal rats. The results are as follows: (1) ketamine injected intraperitoneally (i.p.) 15min prior to EA enhanced the antinociceptive effects of 100 Hz EA at a dose of 5.0mg/kg, but not 0.2 or 1.0mg/kg. However, ketamine at either dose did not affect the basal nociceptive threshold (represented by tail-flick latency). (2) Ketamine at a dose of 5.0mg/kg delayed the development of chronic tolerance to 100Hz EA antinociception. We conclude that ketamine can enhance antinociception of 100Hz EA and delay the tolerance to 100Hz EA in rats. These results suggest that the development of 100Hz EA tolerance to antinociception was mediated, at least in part, through peripheral NMDA receptors, which may be useful in improving the therapeutic effects of EA in the treatment of pain when EA tolerance occurs.