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首页> 外文期刊>The European Journal of Neuroscience >Synaptic plasticity in the acoustic startle pathway: the neuronal basis for short-term habituation?
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Synaptic plasticity in the acoustic startle pathway: the neuronal basis for short-term habituation?

机译：听觉惊吓途径中的突触可塑性：短期习惯的神经元基础？

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The aim of the present study was to analyse the cellular mechanism underlying short-term habituation of the acoustic startle response (ASR). We explored distinct synapses of the neuronal startle pathway in rat brain slices by patch-clamp recordings of giant neurons in the caudal pontine reticular formation. Presynaptic stimulation of auditory afferents by repeated bursts at 0.1 and 1 Hz led to an exponential decay of EPSC magnitudes. This homosynaptic depression (HSD) was reversible and repeatedly inducible after recovery. Many parameters of HSD in vitro match those of ASR habituation in vivo. The mechanisms underlying HSD are distinct from classical short-term plasticity: paired-pulse as well as paired-burst stimulation revealed a facilitation of the second EPSC, occurring in a much smaller time window up to interstimulus intervals of 200 ms. Pharmacological experiments demonstrated that HSD could be completely blocked by the group II and III metabotropic glutamate receptor antagonist MPPG. Similar results were obtained by CPPG, another group II and III antagonist. In contrast, HSD was not affected by the group I and II antagonist MCPG. We conclude that we found a form of synaptic depression in synapses within the primary startle pathway which correlates in many respects with short-term habituation of the ASR and which is presumably mediated by group III metabotropic glutamate receptors.
机译：本研究的目的是分析声惊吓反应（ASR）的短期适应的细胞机制。我们通过尾神经桥网状结构中巨大神经元的膜片钳记录来探索大鼠脑片中神经元惊吓途径的不同突触。突触对突触前突触的刺激以0.1和1 Hz的反复爆发导致EPSC幅度的指数衰减。此同突触抑制（HSD）是可逆的，恢复后可反复诱发。体外HSD的许多参数与体内ASR适应的参数相匹配。 HSD的潜在机制与经典的短期可塑性不同：成对脉冲以及成对突发刺激显示出第二个EPSC的促进作用，发生在一个较小的时间窗口内，直至200 ms的刺激间隔。药理实验表明，HSD可被II和III组代谢型谷氨酸受体拮抗剂MPPG完全阻断。 CPPG（另一组II和III组拮抗剂）获得了相似的结果。相反，HSD不受I和II组拮抗剂MCPG的影响。我们得出的结论是，我们在初级惊吓途径中的突触中发现了一种突触抑制的形式，该突触抑制在许多方面与ASR的短期习性相关，并且大概是由III组代谢型谷氨酸受体介导的。

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