Suwabe Takeshi, Fukami Hideyuki, Bradley Robert M
Department of Biologic and Materials Sciences, School of Dentistry, University of Michigan, Ann Arbor, MI 48109-1078, USA.
J Neurophysiol. 2008 Mar;99(3):1267-73. doi: 10.1152/jn.01115.2007. Epub 2008 Jan 16.
Salivary secretion results from reflex stimulation of autonomic neurons via afferent sensory information relayed to neurons in the rostral nucleus of the solitary tract (rNST), which synapse with autonomic neurons of the salivatory nuclei. We investigated the synaptic properties of the afferent sensory connection to neurons in the inferior salivatory nucleus (ISN) controlling the parotid and von Ebner salivary glands. Mean synaptic latency recorded from parotid gland neurons was significantly shorter than von Ebner gland neurons. Superfusion of GABA and glycine resulted in a concentration-dependent membrane hyperpolarization. Use of glutamate receptor antagonists indicated that both AMPA and N-methyl-D-aspartate (NMDA) receptors are involved in the evoked excitatory postsynaptic potentials (EPSPs). Inhibitory postsynaptic potential (IPSP) amplitude increased with higher intensity ST stimulation. Addition of the glycine antagonist strychnine did not affect the amplitude of the IPSPs significantly. The GABA(A) receptor antagonist, bicuculline (BMI) or mixture of strychnine and BMI abolished the IPSPs in all neurons. IPSP latency was longer than EPSP latency, suggesting that more than one synapse is involved in the inhibitory pathway. Results show that ISN neurons receive both excitatory and inhibitory afferent input mediated by glutamate and GABA respectively. The ISN neuron response to glycine probably derives from descending connections. Difference in the synaptic characteristics of ISN neurons controlling the parotid and von Ebner glands may relate to the different function of these two glands.
唾液分泌是通过传入感觉信息对自主神经元进行反射性刺激而产生的，这些感觉信息传递至孤束核吻侧部（rNST）的神经元，后者与唾液核的自主神经元形成突触。我们研究了支配腮腺和味腺的下唾液核（ISN）中神经元的传入感觉连接的突触特性。从腮腺神经元记录到的平均突触潜伏期显著短于味腺神经元。用γ-氨基丁酸（GABA）和甘氨酸灌流导致浓度依赖性的膜超极化。使用谷氨酸受体拮抗剂表明，α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）受体和N-甲基-D-天冬氨酸（NMDA）受体均参与诱发的兴奋性突触后电位（EPSP）。抑制性突触后电位（IPSP）的幅度随更高强度的三叉神经（ST）刺激而增加。添加甘氨酸拮抗剂士的宁对IPSP的幅度没有显著影响。GABA(A)受体拮抗剂荷包牡丹碱（BMI）或士的宁与BMI的混合物可消除所有神经元中的IPSP。IPSP潜伏期长于EPSP潜伏期，提示抑制性通路涉及不止一个突触。结果表明，ISN神经元分别接受由谷氨酸和GABA介导的兴奋性和抑制性传入输入。ISN神经元对甘氨酸的反应可能源自下行连接。控制腮腺和味腺的ISN神经元突触特征的差异可能与这两种腺体的不同功能有关。
