The purpose of this study is to prove how magnetic field (MF) acts on sympathetic neuro-transmissions using thermal response. Mice were divided into two groups and each one was exposed to MF (20 G, 24 hrs) or sham. Every vehicle or drugs were treated a half hour before the thermal response test. The pain threshold was lowered by MF (20 G, 24 hrs) alone. This reduction of pain threshold by MF was not blocked by a single treatment of $alpha$-receptor antagonist (prazosin), $alpha$$_2$-receptor agonist (clonidine, guanabenz), $eta$$_1$-receptor antagonist (atenolol) or $eta$$_1$,$eta$$_2$-receptor antagonist (propranolol). But administration of $alpha$$_2$-receptor antagonist (yohimbine) completely inhibited the decrease in pain threshold by MF. Moreover, it increased by high dose of yohimbine over normal condition. These results suggest that MF acts on sympathetic nerve terminal to induce hyperalgesia, in which pre-synaptic az receptor might be involved. magnetic field, $alpha$$_2$-receptor, hyperalgesia