Figure 6. Different doses of antagonists into the bilateral thalamic VM nuclei on dexmedetomidine‐induced effects on mechanically and heat‐evoked paw withdrawal reflexes .

Effects of intracerebral (i.c.) administration of different doses of antagonists, atipamezole (Atipa.: 2–10 μg) and WAY‐100635 (WAY.: 0.5–2 μg) into the bilateral thalamic VM nuclei on i.p. dexmedetomidine‐ (Dex, 5 μg kg⁻¹) induced effects on mechanically (A and B) and heat (C and D) evoked paw withdrawal reflexes. All antagonists including vehicle (0.9% saline) were administrated 1 day after the i.p. injection of Dex. Atipamezole and WAY‐100635 dose‐dependently reduced Dex‐induced heat hypoalgesia, suggesting that the second phase of heat hypoalgesia following the treatment with Dex is controlled by endogenous descending noradrenergic and serotonergic pathways. In contrast to the blocking effects on heat hypoalgesia, no effects of these antagonists on mechanically evoked paw withdrawal reflexes were observed. *P < 0.05 and **P < 0.001 compared with the vehicle (i.c. 0.9% saline) treatment (n = 10 for each group). BO, baseline responses before the I.C. Catheterization; B, baseline responses before the i.p. administration of Dex.