Li Tzu-Ling, Chiou Lih-Chu, Lin You Shuei, Hsieh Jing-Ru, Hwang Ling-Ling
Department of Physiology, College of Medicine, Taipei Medical University, Taipei, Taiwan
Am J Physiol Regul Integr Comp Physiol. 2007 Jun;292(6):R2136-43. doi: 10.1152/ajpregu.00563.2006. Epub 2007 Feb 15.
Immunoreactivity of leptin receptor (Ob-R) has been detected in rat dorsal motor nucleus of the vagus (DMNV). Here, we confirmed the presence of Ob-R immunoreactivity on retrograde-labeled parasympathetic preganglionic neurons in the DMNV of neonatal rats. The present study investigated the effects of leptin on DMNV neurons, including parasympathetic preganglionic neurons, by using whole cell patch-clamp recording technique in brain stem slices of neonatal rats. Leptin (30-300 nM) induced membrane depolarization and hyperpolarization, respectively, in 14 and 15 out of 80 DMNV neurons tested. Both leptin-induced inward and outward currents persisted in the presence of TTX, indicating that leptin affected DNMV neurons postsynaptically. The current-voltage (I-V) curve of leptin-induced inward currents is characterized by negative slope conductance and has an average reversal potential of -90 +/- 3 mV. The reversal potential of the leptin-induced inward current was shifted to a more positive potential level in a high-potassium medium. These results indicate that a decrease in potassium conductance is likely the main ionic mechanism underlying the leptin-induced depolarization. On the other hand, the I-V curve of leptin-induced outward currents is characterized by positive slope conductance and has an average reversal potential of -88 +/- 3 mV, suggesting that an increase in potassium conductance may underlie leptin-induced hyperpolarization. Most of the leptin-responsive DMNV neurons were identified as being parasympathetic preganglionic neurons. These results suggest that the DMNV is one of the central target sites of leptin, and leptin can regulate parasympathetic outflow from the DMNV by directly acting on the parasympathetic preganglionic neurons of the DMNV.
在大鼠迷走神经背核(DMNV)中已检测到瘦素受体(Ob-R)的免疫反应性。在此,我们证实了新生大鼠DMNV中逆行标记的副交感神经节前神经元上存在Ob-R免疫反应性。本研究通过在新生大鼠脑干切片中使用全细胞膜片钳记录技术,研究了瘦素对DMNV神经元(包括副交感神经节前神经元)的影响。在测试的80个DMNV神经元中,瘦素(30 - 300 nM)分别在14个和15个神经元中诱导了膜去极化和超极化。在存在河豚毒素(TTX)的情况下,瘦素诱导的内向和外向电流均持续存在,这表明瘦素在突触后影响DMNV神经元。瘦素诱导的内向电流的电流-电压(I-V)曲线具有负斜率电导的特征,平均反转电位为-90±3 mV。在高钾培养基中,瘦素诱导的内向电流的反转电位向更正的电位水平移动。这些结果表明钾电导降低可能是瘦素诱导去极化的主要离子机制。另一方面,瘦素诱导的外向电流的I-V曲线具有正斜率电导的特征,平均反转电位为-88±3 mV,这表明钾电导增加可能是瘦素诱导超极化的基础。大多数对瘦素反应的DMNV神经元被鉴定为副交感神经节前神经元。这些结果表明,DMNV是瘦素的中枢靶位点之一,瘦素可通过直接作用于DMNV的副交感神经节前神经元来调节从DMNV发出的副交感神经传出。