[Met5]enkephalin and delta2-opioid receptors in the spinal cord are involved in the cold water swimming-induced antinociception in the mouse.

Mice made cold water swimming (CWS: 4 degrees C, 3 min) produced an opioid-mediated antinociception. Experiments were designed to determine what types of opioid receptors and endogenous opioid peptides in the spinal cord are involved in the CWS-induced antinociception in male ICR mice. Antinociception was measured by the tail-flick test. CWS-induced antinociception was blocked by intrathecal (i.t.) pretreatment with antiserum to [Met5]enkephalin (100 microg, 1 hr), but not by antiserum (100 microg, 1 hr) to [Leu5]enkephalin, beta-endorphin or dynorphin A (1-17). Moreover, i.t. pretreatment with delta2-opioid receptor antagonist naltriben (NTB: 10 microg, 10 min) blocked the antinociception induced by CWS or i.t.-administered [Met5]enkephalin (10 microg). However, the antinociception induced by CWS or i.t.-administered [Met5]enkephalin was not blocked by i.t. pretreatment with delta1-opioid receptor antagonist 7-benzylidene naltrexone (BNTX: 1 microg, 10 min), mu-opioid receptor antagonist D-Phe-Cys-Try-D-Try-Om-Thr-Phe-Thr-NH2 (CTOP: 50 ng, 10 min), or kappa-opioid receptor antagonist norbinaltorphimine (norBNI: 5 microg, 24 hr). These data indicate that [Met5]enkephalin and delta2-opioid receptor in the spinal cord are involved in antinociception induced by CWS.