Objective To investigate whether the peri pheral administration of amitri ptyl ine produces antihyperalgesiceffect following the chronic constriction injury (CCI) of the sciatic nerve in rats. Methods Forty-eight maleCCI rats weighing (220 ± 20) g were randomly divided into 6 groups (n=8)：group NS, group A2.5, group A5, group A10,group A15.9 and group Aip. In the group NS, group A2.5, group A5, group A10 and group A15.9, sciatic nerve blockade was locally performed with 0.5 mL normal sal ine, and 2.5, 5.0, 10.0, 15.9 mmol/L amitriptyl ine respectively through implanted cannulas on the 7th day after operation. In the group Aip, amitriptyl ine (2.5 mg) was administered by intraperitoneal injection. The mechanical withdrawal threshold (MWT), thermal withdrawal latency (TWL) and motor function were measured before and 1, 2, 4, 8, 12, 24 and 48 hours after sciatic nerve blockade. Results Forty-eight CCI rats were all survival without infection palsy and catheter fall ing off. The rats of group A2.5, group NS and group Aip didn’t produce ambulation deficits. There were no significant difference in these 3 groups (P gt; 0.05). However compared with group A2.5, group NS and group Aip, the rats of group A5, group A10, group A15.9 all produced significant ambulation deficits (P lt; 0.05). The ambulation deficits lasted 2 hours (group A5), 4 hours (group A10), 8 hours (group A15.9) respectively. But the ambulation deficits of CCI rats were all reversible. The MWT and TWL of groups with local injection of amitriptyl ine increased when conpared with group NS, group Aip and those of before injection (P lt; 0.05). Sciatic nerve blockade with amitriptyl ine significantly suppressed mechanical hyperalgesia and thermal hyperalgesia in neuropathic rats. The peripheral anti-hyperalgesic effects lasted 2 hours (A2.5 group), 4 hours (group A5), 24 hours (group A10), 24 hours (group A15.9) respectively. But there were no significant difference between A10 group and A15.9 group (P gt; 0.05). There were no significant difference between group NS and group Aip (P gt; 0.05). Conclusion The peri pheral anti-hyperalgesic effects can be found in sciatic nerve blockade of amitri ptyl ine on CCI rats. And this effect of amitri ptyl ine has concentration dependent and ceil ing effect. Amitri ptyl ine of 5.0-15.9 mmol/L can produce significantambulation deficits which are reversible.
Neuropathic pain has been redefined by NeuPSIG as “pain arising as a direct consequence of a lesion or disease affecting the somatosensory syste”. However, pharmacological management for neuropathic pain is not effective, which is correlated with the uncertainty of pathogenesis. For a long time, neuron had been considered acting a major role in the development of neuropathic pain. In recent years, a majority of studies revealed that glia cell also involved in the occurrence and development of neuropathic pain, and neuron-glia interaction is one of the key mechanism of neuropathic pain, including complex signaling pathways as purinergic signaling. This review focuses on recent advances on the role of purinergic receptors in neuropathic pain.