To determine whether neuronal nitric oxide synthase (nNOS) is involved in nicotine-induced behavioral sensitization in μ-opioid receptor knockout mice we adopted an immunohistochemical approach. Our results confirm that repeated nicotine administration increased locomotor activity in wild-type mice, but failed to increase locomotor activity in μ-opioid receptor knockout mice, thus suggesting that the μ-opioid receptor is involved in behavioral sensitization. Higher numbers of nNOS-positive cells were observed in the striatum of wild-type mice repeatedly treated with nicotine than in saline-treated wild-type mice. However, μ-opioid receptor knockout mice showed significantly lower nicotine-induced nNOS expression in the striatum versus wild-type mice. No differences were found in the hilus of the dentate gyrus between wild-type and μ-opioid receptor knockout mice. These findings demonstrate that the absence of μ-opioid receptors can cause a significant reduction in the expression of nNOS in the striatum, as induced by repeated nicotine treatment.
Bibliographical noteFunding Information:
This research was supported by a grant (M103KV01000804K220100830) from the Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology, Republic of Korea.
- Knockout mice
- μ-Opioid receptors