Simons-Weidenmaier Nadine S, Weber Maruschka, Plappert Claudia F, Pilz Peter K D, Schmid Susanne
Tierphysiologie, Zoologisches Institut, Fakultät für Biologie, Universität Tübingen, Auf der Morgenstelle 28, 72076 Tübingen, Germany.
BMC Neurosci. 2006 May 9;7:38. doi: 10.1186/1471-2202-7-38.
Short-term habituation of the startle response represents an elementary form of learning in mammals. The underlying mechanism is located within the primary startle pathway, presumably at sensory synapses on giant neurons in the caudal pontine reticular nucleus (PnC). Short trains of action potentials in sensory afferent fibers induce depression of synaptic responses in PnC giant neurons, a phenomenon that has been proposed to be the cellular correlate for short-term habituation. We address here the question whether both this synaptic depression and the short-term habituation of the startle response are localized at the presynaptic terminals of sensory afferents. If this is confirmed, it would imply that these processes take place prior to multimodal signal integration, rather than occurring at postsynaptic sites on PnC giant neurons that directly drive motor neurons.
Patch-clamp recordings in vitro were combined with behavioral experiments; synaptic depression was specific for the input pathway stimulated and did not affect signals elicited by other sensory afferents. Concordant with this, short-term habituation of the acoustic startle response in behavioral experiments did not influence tactile startle response amplitudes and vice versa. Further electrophysiological analysis showed that the passive properties of the postsynaptic neuron were unchanged but revealed some alterations in short-term plasticity during depression. Moreover, depression was induced only by trains of presynaptic action potentials and not by single pulses. There was no evidence for transmitter receptor desensitization. In summary, the data indicates that the synaptic depression mechanism is located presynaptically.
Our electrophysiological and behavioral data strongly indicate that synaptic depression in the PnC as well as short-term habituation are located in the sensory part of the startle pathway, namely at the axon terminals of sensory afferents in the PnC. Our results further corroborate the link between synaptic depression and short-term habituation of the startle response.
惊吓反应的短期习惯化是哺乳动物学习的一种基本形式。其潜在机制位于初级惊吓通路内，推测在尾侧脑桥网状核（PnC）中巨型神经元的感觉突触处。感觉传入纤维中的短串动作电位会导致PnC巨型神经元突触反应的抑制，这一现象被认为是短期习惯化的细胞对应物。我们在此探讨这一突触抑制以及惊吓反应的短期习惯化是否都定位于感觉传入神经的突触前终末。如果得到证实，这将意味着这些过程发生在多模式信号整合之前，而非发生在直接驱动运动神经元的PnC巨型神经元的突触后位点。
体外膜片钳记录与行为实验相结合；突触抑制对所刺激的输入通路具有特异性，并不影响其他感觉传入神经引发的信号。与此一致的是，行为实验中听觉惊吓反应的短期习惯化并不影响触觉惊吓反应的幅度，反之亦然。进一步的电生理分析表明，突触后神经元的被动特性未发生改变，但在抑制过程中短期可塑性出现了一些变化。此外，抑制仅由突触前动作电位串诱导，而非单个脉冲。没有证据表明递质受体脱敏。总之，数据表明突触抑制机制位于突触前。
我们的电生理和行为数据有力地表明，PnC中的突触抑制以及短期习惯化位于惊吓通路的感觉部分，即在PnC中感觉传入神经的轴突终末处。我们的结果进一步证实了突触抑制与惊吓反应短期习惯化之间的联系。
