Analysis of the role of inhibition in shaping responses to sinusoidally amplitude-modulated signals in the inferior colliculus
Analysis of the role of inhibition in shaping responses to sinusoidally amplitude-modulated signals in the inferior colliculus
复制标题
DOI：
10.1152/jn.1998.80.4.1686
复制
发表时间：
1998-10-01
影响因子：
2.5
通讯作者：
Pollak, GD
中科院分区：
文献类型：
--
作者：
Burger, RM;Pollak, GD
下丘中央核（ICc）的神经元通常对低频率的正弦幅度调制（SAM）信号产生锁相放电反应，而对较高的SAM频率则不能锁相。以往的研究表明，相当的锁相SAM发生在背核的外侧丘系（DNLL）和内侧上级橄榄（MSO）的胡子蝙蝠。MSO和DNLL的研究还表明，低SAM速率的受限锁相是由具有略微不同的延迟的锁相兴奋性和抑制性输入的重合产生的。在这里，我们测试了这一假设，即在胡子蝙蝠IC SAM的反应是由相同的机制，形状SAM在两个较低的核团的反应。我们记录了在离子电渗应用几种药物之前和期间SAM信号诱发的ICc神经元的反应：荷包牡丹碱，γ-氨基丁酸-A（GABA（A））受体的竞争性拮抗剂;士的宁，甘氨酸受体的竞争性拮抗剂; GABAB受体阻断剂，法氯芬和N-甲基-D-天冬氨酸（NMDA）受体阻断剂，（-）-2-氨基-5-磷酸戊酸（APS）。抑制作用对ICc中SAM信号的响应形成的假设未得到证实。在>90%的测试的ICc神经元中，它们锁相的SAM率的范围在用荷包牡丹碱、士的宁或phaclofen单独或组合应用的阻断抑制后不变。我们还考虑了更快的α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA）受体遵循高时间速率的传入兴奋，但较慢的NMDA受体只能遵循较低的速率的可能性。因此，在较高的SAM率，NMDA受体可能会产生持续的兴奋，“涂抹”AMPA受体产生的锁相兴奋。与抑制假说一样，NMDA假说也未得到证实。在我们测试的细胞中，单独应用AP 5或与荷包牡丹碱组合应用AP 5都不会引起锁相的SAM速率范围的增加。这些结果表明，相同的响应特性，相位锁定限制在低SAM率，是形成在一个以上的方式在听觉脑干。在MSO和DNLL中，机制是锁相兴奋和抑制的重合，而在ICc中，相同的响应特征由不同但未知的机制形成。
Neurons in the central nucleus of the inferior colliculus (ICc) typically respond with phase-locked discharges to low rates of sinusoidal amplitude-modulated (SAM) signals and fail to phase-lock to higher SAM rates. Previous Studies have shown that comparable phase-locking to SAM occurs in the dorsal nucleus of the lateral lemniscus (DNLL) and medial superior olive (MSO) of the mustache bat. The studies of MSO and DNLL also showed that the restricted phase-locking to low SAM rates is created by the coincidence of phase-locked excitatory and inhibitory inputs that have slightly different latencies. Here we tested the hypothesis that responses to SAM in the mustache bat IC are shaped by the same mechanism that shapes responses to SAM in the two lower nuclei. We recorded responses from ICc neurons evoked by SAM signals before and during the iontophoretic application of several pharmacological agents: bicuculline, a competitive antagonist for gamma-aminobutyric acid-A (GABA(A)) receptors; strychnine, a competitive antagonist for glycine receptors; the GABAB receptor blocker, phaclofen, and the N-methyl-D-aspartate (NMDA) receptor blocker, (-)-2-amino-5-phosphonopentanoic acid(APS). The hypothesis that inhibition shapes responses to SAM signals in the ICc was not confirmed. In >90% of the ICc neurons tested, the range of SAM rates to which they phase-locked was unchanged after blocking inhibition with bicuculline, strychnine or phaclofen, applied either individually or in combination. We also considered the possibility that faster alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors follow high temporal rates of incoming excitation but that the slower NMDA receptors could follow only lower rates. Thus at higher SAM rates, NMDA receptors might generate a sustained excitation that "smears" the phase-locked excitation generated by the AMPA receptors. The NMDA hypothesis, Like the inhibition hypothesis; was also not confirmed. In none of the cells that we tested did the application of AP5 by itself, or in combination with bicuculline, cause an increase in the range of SAM rates that evoked phase-locking. These results illustrate that the same response property, phase-locking restricted to low SAM rates, is formed in more than one way in the auditory brain stem. In the MSO and DNLL, the mechanism is coincidence of phase-locked excitation and inhibition, whereas in ICc the same response feature is formed by a different but unknown mechanism.