Akinola Lois S, Mckiver Bryan, Toma Wisam, Zhu Andy Z X, Tyndale Rachel F, Kumar Vivek, Damaj M Imad
Department of Pharmacology and Toxicology, and Translational Research Initiative for Pain and Neuropathy, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA 23298, USA.
Takeda Pharmaceutical Company Limited, Cambridge, MA 02139, USA.
Brain Sci. 2019 Sep 21;9(10):244. doi: 10.3390/brainsci9100244.
Tobacco smoking is the major cause of disability and death in the United States and around the world. In addition, tobacco dependence and addiction express themselves as complex behaviors involving an interplay of genetics, environment, and psychological state. Mouse genetic studies could potentially elucidate the novel genes and/or gene networks regulating various aspects of nicotine dependence. Using the closely related C57BL/6 (B6) mice substrains, recent reports have noted phenotypic differences within C57BL/6J (B6J) and C57BL/6N (B6N) mice for some drugs of abuse: alcohol, opiates, and cocaine. However, the differences in nicotine's effects have not yet been described in these substrains. We examined the phenotypic differences in these substrains following the acute and repeated administration of nicotine in several pharmacological measures, including locomotion (after acute and repeated exposure), body temperature, nociception, and anxiety-like behaviors. We report substrain differences in the pharmacological effects of acute and repeated nicotine administration in the B6 substrains. Overall, we show enhanced nicotine sensitivity to locomotion, hypothermia, antinociception, and anxiety-like behaviors in the B6J mouse substrain compared to B6N. In the repeated administration paradigm, both the B6N and B6J substrains showed no sensitized locomotor responses after repeated exposure to nicotine at the two doses tested. This study thus provides evidence that the B6 mouse substrains may be useful for genetic studies to elucidate some of the genetic variants involved in tobacco dependence and addiction.
吸烟是美国乃至全世界残疾和死亡的主要原因。此外,烟草依赖和成瘾表现为复杂的行为,涉及基因、环境和心理状态的相互作用。小鼠遗传学研究有可能阐明调节尼古丁依赖各个方面的新基因和/或基因网络。利用密切相关的C57BL/6(B6)小鼠亚系,最近的报告指出,在C57BL/6J(B6J)和C57BL/6N(B6N)小鼠中,对于某些滥用药物(酒精、阿片类药物和可卡因)存在表型差异。然而,这些亚系中尼古丁作用的差异尚未得到描述。我们通过几种药理学指标,包括运动能力(急性和反复暴露后)、体温、痛觉感受和焦虑样行为,研究了这些亚系在急性和反复给予尼古丁后的表型差异。我们报告了B6亚系中急性和反复给予尼古丁的药理学效应存在亚系差异。总体而言,我们发现与B6N相比,B6J小鼠亚系对尼古丁引起的运动能力增强、体温过低、抗痛觉感受和焦虑样行为更为敏感。在反复给药模式中,B6N和B6J亚系在测试的两种剂量下反复暴露于尼古丁后,均未表现出运动反应敏感化。因此,本研究提供了证据,表明B6小鼠亚系可能有助于进行遗传学研究,以阐明一些与烟草依赖和成瘾有关的基因变异。