关键词: Arcuate FOS Hypothalamus POMC Rodent Self-administration

Mesh : Animals Nicotine / pharmacology Male Brain / drug effects metabolism Rats Rats, Sprague-Dawley Nicotinic Agonists / pharmacology Feeding Behavior / drug effects Pro-Opiomelanocortin / metabolism Eating / drug effects physiology Self Administration Neurons / drug effects metabolism Proto-Oncogene Proteins c-fos / metabolism Anorexia / chemically induced

来  源:   DOI:10.1016/j.neuropharm.2024.109959

Abstract:
Nicotine use produces psychoactive effects, and chronic use is associated with physiological and psychological symptoms of addiction. However, chronic nicotine use is known to decrease food intake and body weight gain, suggesting that nicotine also affects central metabolic and appetite regulation. We recently showed that acute nicotine self-administration in nicotine-dependent animals produces a short-term increase in food intake, contrary to its long-term decrease of feeding behavior. As feeding behavior is regulated by complex neural signaling mechanisms, this study aimed to test the hypothesis that nicotine intake in animals exposed to chronic nicotine may increase activation of pro-feeding regions and decrease activation of pro-satiety regions to produce the acute increase in feeding behavior. FOS immunohistochemistry revealed that acute nicotine intake in nicotine self-administering animals increased activation of the pro-feeding arcuate and lateral hypothalamic nuclei and decreased activation of the pro-satiety parabrachial nucleus. Regional correlational analysis also showed that acute nicotine changes the functional connectivity of the hunger/satiety network. Further dissection of the role of the arcuate nucleus using electrophysiology found that putative POMC neurons in animals given chronic nicotine exhibited decreased firing following acute nicotine application. These brain-wide central signaling changes may contribute to the acute increase in feeding behavior we see in rats after acute nicotine and provide new areas of focus for studying both nicotine addiction and metabolic regulation.
摘要:
使用尼古丁会产生精神作用,长期使用与成瘾的生理和心理症状有关。然而,众所周知,长期使用尼古丁会减少食物摄入量和体重增加,这表明尼古丁也影响中枢代谢和食欲调节。我们最近表明,尼古丁依赖动物的急性尼古丁自我管理会导致食物摄入量的短期增加,与其长期减少的摄食行为相反。由于进食行为受复杂的神经信号机制调节,这项研究旨在检验以下假设:暴露于慢性尼古丁的动物的尼古丁摄入可能会增加促摄食区的激活和减少促饱腹区的激活,从而导致摄食行为的急性增加.FOS免疫组织化学显示,尼古丁自我给药动物的急性尼古丁摄入量增加了前进食弓形和下丘脑外侧核的激活,并减少了前饱腹性臂旁核的激活。区域相关分析还表明,急性尼古丁改变了饥饿/饱腹感网络的功能连通性。使用电生理学进一步解剖弓状核的作用发现,给予慢性尼古丁的动物中推定的POMC神经元在急性尼古丁施用后表现出降低的放电。这些全脑中枢信号的变化可能有助于我们在急性尼古丁后的大鼠中看到的喂养行为的急性增加,并为研究尼古丁成瘾和代谢调节提供了新的重点领域。
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