2P200 Intrathecal clonidine inhibits nrechanical allodynia via the spinal muscarinic M1 receptors in diabetic mice

• Published in: Journal of Pharmacological Sciences 2003, Vol.91 (suppl.1), p.186-186
• Main Authors: Kohei Koga, Kenji Honda, Suguru Ando, Masako Koguchi, Ryo Saito, Hiro-o Kamiya, Yukio Takano
• Format: Article
• Language: Japanese
• ISSN: 1347-8613

We reported previously that intrathecal (i, t. ) α2 agonist clonidine inhibits mechanical transmission via the muscarinic M I receptors in the spinal cord (Honda et al., Neurosci. Lett., 322, 161-164, 2002). In this study, we examined the possible involvement of the muscarinic receptors in the anti-allodynia effect of clonidine in diabetic mice. The diabetic mice were obtained by intravenous injection of streptozotocine (STZ). Mechanical allodynia was assessed by using von Frey filament. The mechanical allodynia was produced by STZ-induced diabetic mice. The allodynia was inhibited by i. t, injection of clonidine. The i. t. injection of α2 antagonist yohimbine inhibited clonidine-induced anti-allodynic effect. The clonidine-induced anti-allodynic effect was also blocked by atropine (i. t. ) and muscarinic M1 antagonist pirenzepine (i, t. ), but not by the M2 antagonist methoctramine and M3 antagonist 4-DAMP. In addition, i. t. injection of M1 agonist McN-A-343 inhibited the mechanical allodynia. These results suggest that intrathecal clonidine inhibits diabete-induced mechanical allodynia via the activating muscarinic M1 receptors in the spinal cord in mice.