Scholl Ben, Wehr Michael
Institute of Neuroscience, University of Oregon, Eugene, OR 97403, USA.
J Neurophysiol. 2008 Aug;100(2):646-56. doi: 10.1152/jn.90406.2008. Epub 2008 Jun 4.
Sensory deafferentation results in rapid shifts in the receptive fields of cortical neurons, but the synaptic mechanisms underlying these changes remain unknown. The rapidity of these shifts has led to the suggestion that subthreshold inputs may be unmasked by a selective loss of inhibition. To study this, we used in vivo whole cell recordings to directly measure tone-evoked excitatory and inhibitory synaptic inputs in auditory cortical neurons before and after acoustic trauma. Here we report that acute acoustic trauma disrupted the balance of excitation and inhibition by selectively increasing and reducing the strength of inhibition at different positions within the receptive field. Inhibition was abolished for frequencies far below the trauma-tone frequency but was markedly enhanced near the edges of the region of elevated peripheral threshold. These changes occurred for relatively high-level tones. These changes in inhibition led to an expansion of receptive fields but not by a simple unmasking process. Rather, membrane potential responses were delayed and prolonged throughout the receptive field by distinct interactions between synaptic excitation and inhibition. Far below the trauma-tone frequency, decreased inhibition combined with prolonged excitation led to increased responses. Near the edges of the region of elevated peripheral threshold, increased inhibition served to delay rather than abolish responses, which were driven by prolonged excitation. These results show that the rapid receptive field shifts caused by acoustic trauma are caused by distinct mechanisms at different positions within the receptive field, which depend on differential disruption of excitation and inhibition.
感觉传入神经切断导致皮质神经元感受野迅速发生变化，但其变化背后的突触机制仍不清楚。这些变化的快速性使人推测阈下输入可能因抑制性输入的选择性丧失而被暴露出来。为了研究这一点，我们利用在体全细胞记录技术，直接测量声创伤前后听觉皮质神经元中音调诱发的兴奋性和抑制性突触输入。我们在此报告，急性声创伤通过选择性地增强和减弱感受野内不同位置的抑制强度，破坏了兴奋与抑制之间的平衡。对于远低于创伤音调频率的频率，抑制作用消失，但在周边阈值升高区域的边缘附近，抑制作用明显增强。这些变化发生在相对高强度的音调情况下。抑制作用的这些变化导致感受野扩大，但并非通过简单的暴露过程。相反，在整个感受野中，突触兴奋与抑制之间的独特相互作用使膜电位反应延迟并延长。在远低于创伤音调频率时，抑制作用减弱与兴奋作用延长相结合导致反应增强。在周边阈值升高区域的边缘附近，抑制作用增强起到延迟而非消除反应的作用，反应由延长的兴奋驱动。这些结果表明，声创伤引起的快速感受野变化是由感受野内不同位置的独特机制引起的，这取决于兴奋与抑制的差异性破坏。
