神经性厌食症大鼠伏隔核与延髓头端腹外侧区的神经通路联系

Neural pathway between the nucleus accumbens and the rostral ventrolateral medulla in a rat model of anorexia nervosa

目的探讨中枢伏隔核(NAc)与延髓头端腹外侧区(RVLM)之间是否存在神经通路联系,为进一步阐明神经性厌食症(AN)患者心血管功能的中枢调节机制提供新的理论依据。方法采用饮食-运动模拟法建立神经性厌食症大鼠模型,使用荧光金逆向示踪法并结合多通道同步记录技术,探究NAc与RVLM间是否存在通路联系并参与AN模型大鼠心血管功能的调节。结果与正常对照组相比,AN模型组大鼠收缩压、平均动脉压和心率显著降低,RVLM神经元放电频率显著增加。在正常组和AN模型组大鼠RVLM核团微量注射荧光金0.5μL后,观察到NAc有荧光金逆行标记神经元分布。400μA电刺激正常组和模型组大鼠NAc时,大鼠收缩压、心率均显著性降低,RVLM神经元放电频率显著增加,而电刺激后模型组的舒张压、平均动脉压明显低于正常组。结论应用饮食-运动模拟法能成功建立神经性厌食症大鼠模型。大鼠NAc与RVLM间存在神经通路联系,该神经通路可能参与了AN模型大鼠心血管功能的调节。

Objective To investigate the potential neural pathway connecting the nucleus accumbens(NAc)and the rostral ventrolateral medulla(RVLM),and whether the pathway participates in the regulation of cardiovascular function in a model rat of anorexia nervosa(AN).Methods Rat models of AN were established by allowing voluntary activity in a running wheel with restricted feeding,with the rats having free access to normal chow without exercise as the control group.FluoroGold(FG)retrograde tracing method and multi-channel simultaneous recording technique were used to explore the possible pathway between the NAc and the RVLM.Results The rats inAN group exhibited significantly reduced systolic blood pressure(SBP),mean arterial pressure(MAP)and heart rate(HR)with significantly increased discharge frequency of RVLM neurons in comparison with the control rats.After the injection of FG into the RVLM,retrograde labeled neuronswere observed in the NAc of the rats in both the normal control and AN groups.In both groups,SBP and HR were significantly decreased in response to 400μA electrical stimulation of the NAc accompanied by an obvious increase in the discharge frequency of the RVLM neurons;the diastolic blood pressure(DBP)and MAP were significantly lower in AN model rats than in the normal rats in response to the stimulation.ConclusionsWe successfully established a rat model of AN via hyperactivity and restricted feeding and confirm the presence of a neural pathway connecting the NAc and the RVLM.This pathway might participate in the regulation of cardiovascular function in ANmodel rats.