Met 5]enkephalin and δ2-opioid receptors in the spinal cord are involved in the cold water swimming-induced antinociception in the mouse

Abstract

Mice made cold water swimming (CWS: 4 °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 [Met 5]enkephalin (100 μg, 1 hr), but not by antiserum (100 μg, 1 hr) to [Leu 5]enkephalin, β-endorphin or dynorphin A (1–17). Moreover, i.t. pretreatment with δ 2-opioid receptor antagonist naltriben (NTB: 10 μg, 10 min) blocked the antinociception induced by CWS or i.t.-administered [Met 5]enkephalin (10 μg). However, the antinociception induced by CWS or i.t.-administered [Met 5]enkephalin was not blocked by i.t. pretreatment with δ 1-opioid receptor antagonist 7-benzylidene naltrexone (BNTX: 1 μg, 10 min), μ-opioid receptor antagonist d-Phe-Cys-Try- d-Try-Orn-Thr-Phe-Thr-NH 2 (CTOP: 50 ng, 10 min), or κ-opioid receptor antagonist norbinaltorphimine (norBNI: 5 μg, 24 hr). These data indicate that [Met 5]enkephalin and δ 2-opioid receptor in the spinal cord are involved in antinociception induced by CWS.