Paton J F, Li Y W, Schwaber J S
Department of Physiology, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, UK.
Ann N Y Acad Sci. 2001 Jun;940:157-68. doi: 10.1111/j.1749-6632.2001.tb03674.x.
Neurons in the nucleus of the solitary tract (NTS) responding to activation of arterial baroreceptors were recorded intracellularly using patch pipettes in an in situ arterially perfused working heart-brain stem preparation of rat. Seven of 15 (i.e., 46%) of NTS neurons showed adaptive (nonlinear) excitatory synaptic response patterns during baroreceptor stimulation followed by an "evoked hyperpolarization." This evoked hyperpolarization was stimulus intensity dependent and capable of shunting out a subsequent baroreceptor input. We suggest that this adaptive response behavior may be mediated, in part, by calcium-dependent potassium currents (IKCa) since neurons showed spike frequency adaptation during step depolarizations and an after-hyperpolarization after repetitive firing. Furthermore, in in vivo anesthetized rats, NTS microinjections of either charybdotoxin (225 fmol) or apamin (4.5 pmol) to block IKCa increased the baroreceptor reflex gain. Our data purport that the responsiveness of baroreceptive NTS neurons can be regulated by intrinsic membrane conductances such as IKCa. Modulation of such conductances during either physiological (exercise) or pathophysiological (essential hypertension) conditions may lead to changes in both the operating point and gain of the baroreceptor reflex.
在大鼠原位动脉灌注工作心脏 - 脑干制备标本中,使用膜片吸管对孤束核(NTS)中对动脉压力感受器激活产生反应的神经元进行细胞内记录。15个NTS神经元中有7个(即46%)在压力感受器刺激期间表现出适应性(非线性)兴奋性突触反应模式,随后出现“诱发超极化”。这种诱发超极化依赖于刺激强度,并且能够分流随后的压力感受器输入。我们认为,这种适应性反应行为可能部分由钙依赖性钾电流(IKCa)介导,因为神经元在阶跃去极化期间表现出动作电位频率适应性,并且在重复放电后出现超极化后电位。此外,在体内麻醉的大鼠中,向NTS微量注射阻断IKCa的美洲商陆毒素(225飞摩尔)或蜂毒明肽(4.5皮摩尔)可增加压力感受器反射增益。我们的数据表明,压力感受性NTS神经元的反应性可由诸如IKCa等内在膜电导调节。在生理(运动)或病理生理(原发性高血压)条件下调节此类电导可能导致压力感受器反射的工作点和增益发生变化。