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首页> 外文期刊>Addiction biology >Nicotine is more addictive, not more cognitively therapeutic in a neurodevelopmental model of schizophrenia produced by neonatal ventral hippocampal lesions
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Nicotine is more addictive, not more cognitively therapeutic in a neurodevelopmental model of schizophrenia produced by neonatal ventral hippocampal lesions

机译：在新生儿腹侧海马损伤产生的精神分裂症的神经发育模型中，尼古丁更具成瘾性，而不是认知治疗

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Nicotine dependence is the leading cause of death in the United States. However, research on high rates of nicotine use in mental illness has primarily explained this co-morbidity as reflecting nicotine's therapeutic benefits, especially for cognitive symptoms, equating smoking with 'self-medication'. We used a leading neurodevelopmental model of mental illness in rats to prospectively test the alternative possibility that nicotine dependence pervades mental illness because nicotine is simply more addictive in mentally ill brains that involve developmental hippocampal dysfunction. Neonatal ventral hippocampal lesions (NVHL) have previously been demonstrated to produce post-adolescent-onset, pharmacological, neurobiological and cognitive-deficit features of schizophrenia. Here, we show that NVHLs increase adult nicotine self-administration, potentiating acquisition-intake, total nicotine consumed and drug seeking. Behavioral sensitization to nicotine in adolescence prior to self-administration is not accentuated by NVHLs in contrast to increased nicotine self-administration and behavioral sensitization documented in adult NVHL rats, suggesting periadolescent neurodevelopmental onset of nicotine addiction vulnerability in the NVHL model. Delivering a nicotine regimen approximating the exposure used in the sensitization and self-administration experiments (i.e. as a treatment) to adult rats did not specifically reverse NVHL-induced cortical-hippocampal-dependent cognitive deficits and actually worsened cognitive efficiency after nicotine treatment stopped, generating deficits that resemble those due to NVHLs. These findings represent the first prospective evidence demonstrating a causal link between disease processes in schizophrenia and nicotine addiction. Developmental cortical-temporal limbic dysfunction in mental illness may thus amplify nicotine's reinforcing effects and addiction risk and severity, even while producing cognitive deficits that are not specifically or substantially reversible with nicotine.
机译：在美国，尼古丁依赖性是主要的死亡原因。但是，有关在精神疾病中高使用尼古丁的研究主要解释了这种并发症反映了尼古丁的治疗益处，特别是对于认知症状，将吸烟等同于“自我药物治疗”。我们使用了大鼠精神疾病的领先神经发育模型来前瞻性地测试尼古丁依赖性弥漫性精神疾病的另一种可能性，因为尼古丁对涉及发育性海马功能障碍的精神病患者的大脑更容易上瘾。新生儿腹侧海马区病变（NVHL）先前已被证明可导致精神分裂症的青春期发作，药理，神经生物学和认知缺陷特征。在这里，我们显示NVHLs可以提高成人尼古丁的自我管理，增强获取量，总尼古丁消耗量和寻求药物的能力。与成年NVHL大鼠中记录的尼古丁自我管理和行为敏感性增加相比，NVHL并未强调自我管理前青春期对尼古丁的行为敏感性，表明在NVHL模型中青少年期尼古丁成瘾易感性神经发育发作。向成年大鼠提供近似于致敏和自我给药实验（即治疗）中所用暴露的尼古丁方案，并不能特异性逆转NVHL诱导的皮质海马依赖性认知功能障碍，实际上在尼古丁治疗停止后认知效率恶化，产生类似于NVHL的缺陷。这些发现代表了首个前瞻性证据，表明精神分裂症的疾病过程与尼古丁成瘾之间存在因果关系。精神疾病中的发展性皮质-颞叶边缘功能障碍可能会加剧尼古丁的增强作用以及成瘾风险和严重程度，甚至会产生尼古丁无法特异性或基本上可逆的认知缺陷。

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