A presynaptic mechanism contributes to depression of autonomic signal transmission in NTS
A presynaptic mechanism contributes to depression of autonomic signal transmission in NTS
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DOI：
10.1152/ajpheart.1999.277.4.h1350
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发表时间：
1999-10-01
影响因子：
4.8
通讯作者：
Bonham, AC
中科院分区：
文献类型：
--
作者：
Chen, CY;Horowitz, JM;Bonham, AC
随着向孤束核（NTS）的自主神经传入输入频率的增加，突触后反应被抑制。为了验证突触前机制导致频率依赖性抑制的假设，我在NTS切片中使用了全细胞电压钳记录。首先，我们确定孤束刺激（0.4-24 Hz）是否导致二级神经元兴奋性突触后电流（EPSC）的频率依赖性抑制。第二，由于突触前谷氨酸释放的减少导致α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）和N-甲基-D-天冬氨酸（NMDA）受体介导的EPSC组分的平行抑制，我们确定了EPSC组分的幅度、时间过程和从抑制中恢复是否相同。第三，为了确定AMPA受体脱敏是否起作用，我们检查了环噻嗪治疗期间的抑郁。EPSC以频率依赖性的方式减少了76%的第二和92%的高阶神经元。AMPA和NMDA EPSC成分以相同的幅度（83%和83%）和时间常数（113和103 ms）被抑制。恢复的时间常数也没有差异（1.2和0.8 s）。环噻嗪不影响大于或等于3 Hz的突触抑制。这些数据表明，在第一个NTS突触的突触前机制（S）介导的频率依赖性突触抑制。
With increasing frequencies of autonomic afferent input to the nucleus tractus solitarii (NTS), postsynaptic responses are depressed. To test the hypothesis that a presynaptic mechanism contributes to this frequency-dependent depression, me used whole cell, voltage-clamp recordings in an NTS slice. First, we determined whether solitary tract stimulation (0.4-24 Hz) resulted in frequency-dependent depression of excitatory postsynaptic currents (EPSCs) in second-order neurons. Second, because decreases in presynaptic glutamate release result in a parallel depression of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and N-methyl-D-aspartic acid (NMDA) receptor-mediated components of EPSCs, we determined whether the magnitude, time course, and recovery from the depression were the same in both EPSC components. Third, to determine whether AMPA receptor desensitization contributed, we examined the depression during cyclothiazide. EPSCs decreased in a frequency-dependent manner by up to 76% in second- and 92% in higher-order neurons. AMPA and NMDA EPSC components were depressed with the same magnitude (by 83% and 83%) and time constant (113 and 103 ms). The time constant for the recovery was also not different (1.2 and 0.8 s). Cyclothiazide did not affect synaptic depression at greater than or equal to 3 Hz. The data suggest that presynaptic mechanism(s) at the first NTS synapse mediate frequency-dependent synaptic depression.