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首页> 外文期刊>Psychopharmacology >Genotype-dependent effects of adolescent nicotine exposure on dopamine functional dynamics in the nucleus accumbens shell in male and female mice: a potential mechanism underlying the gateway effect of nicotine.
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Genotype-dependent effects of adolescent nicotine exposure on dopamine functional dynamics in the nucleus accumbens shell in male and female mice: a potential mechanism underlying the gateway effect of nicotine.

机译：青春期尼古丁暴露对雄性和雌性小鼠伏隔核壳中多巴胺功能动力学的基因型依赖性影响：尼古丁网关效应的潜在机制。

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RATIONALE: The tendency to use cocaine is determined by genetic and environmental effects across the lifespan. One critical environmental effect is early drug exposure, which is both driven by and interacts with genetic background. The mesoaccumbens dopamine system, which is critically involved in the rewarding properties of drugs of abuse, undergoes significant development during adolescence, and thus may be at particular risk to repeated nicotine exposure during this period, thereby establishing vulnerability for subsequent adult psychostimulant use. OBJECTIVES: We tested the hypotheses that adolescent nicotine exposure results in attenuation of the enhancing effects of cocaine on medial forebrain bundle (MFB) electrical stimulation-evoked dopamine release in the nucleus accumbens shell (AcbSh) in adulthood and that this effect is significantly influenced by genotype. METHODS: Mice from the progenitor strains C57BL/6J and DBA/2J and those from the BXD20/TyJ and BXD86/RwwJ recombinant inbred lines were exposed to nicotine via osmotic minipumps from postnatal day (P) 28 to P56. When mice reached P70, dopamine functional dynamics in AcbSh was evaluated by means of in vivo fixed potential amperometry in combination with electrical stimulation of mesoaccumbens dopaminergic axons in the MFB. RESULTS: Adolescent exposure to nicotine in all strains dose-dependently reduced the ability of a fixed-dose challenge injection of cocaine (10 mg/kg, i.p.) to enhance MFB electrical stimulation-evoked dopamine release in AcbSh in adults. The magnitude of this effect was genotype-dependent. CONCLUSIONS: These results suggest a genotype-dependent mechanism by which nicotine exposure during adolescence causes persistent changes in the sensitivity to "hard" stimulants such as cocaine.
机译：理由：可卡因的使用趋势取决于整个生命周期的遗传和环境影响。一种重要的环境影响是药物的早期暴露，这是由遗传背景驱动并与遗传背景相互作用的。 Mesoaccumbens多巴胺系统（主要涉及滥用药物的奖励性质）在青春期期间经历了显着发展，因此在此期间可能反复暴露于尼古丁，从而为随后的成人使用精神兴奋剂带来了脆弱性。目的：我们测试了以下假说：青春期尼古丁暴露导致可卡因对成年伏隔核壳（AcbSh）中前脑束（MFB）电刺激诱发的多巴胺释放的增强作用减弱，并且这种影响受以下因素的显着影响基因型。方法：从出生后第28天到第56天，通过渗透微型泵将来自祖先菌株C57BL / 6J和DBA / 2J以及来自BXD20 / TyJ和BXD86 / RwwJ重组自交系的小鼠暴露于尼古丁。当小鼠达到P70时，通过体内固定电位安培法结合MFB中的中度累积多巴胺能轴突的电刺激，评估AcbSh中的多巴胺功能动力学。结果：所有菌株的青少年暴露于尼古丁的剂量依赖性降低了可卡因固定剂量激发注射（10 mg / kg，腹腔注射）增强成人AcbSh中MFB电刺激诱发的多巴胺释放的能力。这种作用的程度取决于基因型。结论：这些结果表明，基因型依赖的机制可以使青春期的烟碱暴露引起对“硬”兴奋剂（如可卡因）敏感性的持续变化。

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