Objective: To evaluate the effects of gabapentin and clonidine on neuropathic pain in an experimental pain model.

Method: 24 male adult rats were anesthetized and the sciatic nerve was exposed. Each exposed nerve was electrically injured with 10 volts for 10 seconds by two needle electrodes. Rats were divided into three groups by treating with gabapentin, clonidine and sham. Gabapentin and clonidine were given orally from post operation day 3 to 7 in gabapentin and clonidine groups respectively. To evaluate the presence of mechanical allodynia, withdrawal frequency was tested by Von Frey hair in the same days. After post operation day 7, all the medications were discontinued and mechanical allodynia was evaluated at post operation day 14.

Result: Neuropathic pain was developed after electrical injury in all the rats. Withdrawal frequency is more decreased in gabapentin and clonidine groups than sham group in post operation day 4 to 7. The withdrawal frequency was 2.88⁑0.83, 2.75⁑0.89, 3.13⁑0.99, 3.25⁑1.28 in gabapentin group and 3.38⁑0.92, 4.50⁑2.20, 3.25⁑1.17, 3.50⁑0.93 in clonidine group in post operation day 4, 5, 6, 7, respectively. In post operation day 14, withdrawal frequency was increased and showed no difference compared to the sham group.

Conclusion: Gabapentin and clonidine can suppress the neuropathic pain in an experimental pain model. There was no different effect on the neuropathic pain suppression between gabapentin and clonidine.

Objective: The purpose of this study was to evaluate the anti-inflammatory effect of steroid in the neuroma plays a key role in the development of neuropathic pain.

Method: Materials consisted of 21 male Sprague-Dawley rats (8 weeks old, 180∼200 g), which were divided into a steroid (n=9) and control group (n=12). Neuropathic pain was produced by unilateral transection of the superior caudal trunks at the level between the S3 and S4 spinal nerves. We compared two groups of rats, the steroid group injecting 1 ml (40 mg) of Methylprednisolone (Depo-Medrol), and the control group injecting 1 ml of nomal saline on operation site just after operation.

Behavioral reactions to mechanical allodynia were checked using a von Frey hairs of 2.0 g (19.6 mN) bending force at pre-operation, post-operative 1, 4, 7, 10 & 14 day to evaluate the steroid effect on the development of neuropathic pain.

Results: The steroid group exhibited less tail-flick frequencies to mechanical stimulation: 14.8⁑17.0%, 28.1⁑18.3%, 38.1⁑28.3% at post-operative 4, 7, 10 days respectively in control group; 30.3⁑21.2% 43.6⁑21.3%, 47.2⁑20.8% at post-operative 4, 7, 10 days, respectively. But there was no significant difference between both groups at post-operative 14 days. The steriod reduced the pain at early stage of neuropathic pain development, but failed to decrease the pain level in late stage.

Conclusion: These results suggest that the steroid induced anti-inflammatory effect in the injured neuroma is not a key factor in the development of neuropathic pain.

Objective: In a rat model of peripheral neuropathy, to determine whether neuropathic pain is related to the α-2 adrenergic receptor.

Method: The neuropathic pain was produced by unilateral transection of the superior caudal trunk between the S3 and S4 spinal nerves. These animals showed the behavioral signs of neuropathic pain in the tail. Two weeks after the neuropathic surgery, tail withdrawal responses to the mechanical stimuli with von Frey hair (2.0 g) were examined 1, 2 and 24 hrs following the administration of clonidine, α-2 receptor agonist. One week after the clonidine test, the same behavioral test was done after the administration of clonidine along with yohimbine, α-2 receptor antagonist.

Results: Clonidine significantly reduced the frequency of tail response and yohimbine reversed the clonidine-induced anti-allodynic effect.

Conclusion: These results suggest that neuropathic pain is related to the sympathetic nervous system via α-2 adrenergic receptor.

Objective: The purpose of this study was to evaluate the short- and long-term effects of exercise on neuropathic pain.

Method: Pain responses between rats in the exercise and control groups were compared to evaluate the effects of exercise in neuropathic pain. Materials consisted of 30 male Sprague-Dawley rats (8 weeks old, 180∼200 g), which were divided into an exercise group (n=15) and a control group (n=15). Neuropathic pain was produced by partially injuring the nerve innervating the tail. Running exercise was given on a Rota-rod treadmill exercise machine for 3 weeks (3.1 Km/day, 6 cycle of 9 minutes exercise and 1 minute rest). Behavioral reactions to mechanical allodynia were checked using a von Frey hairs of 2.0 g (19.6 mN) bending force at 10 minutes, 1 hour and 24 hours post-exercise to evaluate the short term effects of exercise. Behavioral reactions to mechanical and thermal allodynia with 4^oC or 40^oC were evaluated 7, 14, 21 and 28 days following exercise.

Result: The exercise group exhibited less tail-flick frequencies to mechanical stimulation from 58.8⁑6.8% to 41.1⁑5.4%, 37.6⁑13.2% at 1 and 24 hours post-exercise compared to the control group, but there was no significant difference between the groups at weeks 1 through 4. In the exercise group, the decrease of tail-flick frequencies were blocked by naloxone (2 mg/kg i.p.). It is suggested that long-lasting muscle exercise (e.g. running) which influences central endorphin mechanisms giving analgetic effects.

Conclusion: The results of this study support the hypothesis that the exercise can reduce neuropathic pain in the acute stage.

Objective: To evaluate the effect of clonidine on the experimental neuropathic pain model and to observe whether neuropathic pain is related to the sympathetic nervous system in this model by reversal of allodynia with administration of epinephrine.

Method: The neuropathic pain was produced by unilateral transection of the superior caudal trunk innervating the rat's tail. Tail withdrawal responses based on mechanical (withdrawal frequency to bending force of von Frey hair 2.0 g) and the thermal (withdrawal latency to tail immersion in a 4^oC or 40^oC water with a cut-off time of 15 seconds) stimuli were used. Experiments were performed two weeks after surgery when neuropathic pain had fully been developed. Experimental group by administration of clonidine was examined by tail withdrawal responses at Day 1, Day 3 and Day 5. After one week of wash-out period, reversal of allodynia by administration of epinephrine was examined by the same test.

Results: Clonidine significantly decreased the frequency of withdrawal with the mechanical stimuli compared with control (P＜0.01), but did not significantly decrease with the cold or warm stimuli. Epinephrine tended to aggravate the mechanical allodynia, but it was not significant compared with the control.

Conclusion: Clonidine may relieve mechanical allodynia in neuropathic pain, but the mechanism of neuropathic pain that is related to the sympathetic nervous system in this experimental model may be unreliable.