Department of Physiology, Third Military Medical University, Chongqing, People's Republic of China;
J Neurophysiol. 2014 May;111(9):1746-58. doi: 10.1152/jn.00180.2013. Epub 2014 Feb 5.
Electrical stimulation of ventral division of medial geniculate body (MGBv) neurons evokes a shift of the frequency-tuning curves of auditory cortical (AC) neurons toward the best frequency (BF) of the stimulated MGBv neurons (frequency-specific plasticity). The shift of BF is induced by inhibition of responses at the BF of the recorded AC neuron, with coincident facilitation of responses at the BF of the stimulated MGBv neuron. However, the synaptic mechanisms are not yet understood. We hypothesize that activation of thalamocortical synaptic transmission and receptor function may contribute to MGBv stimulation-induced frequency-specific auditory plasticity and the shift of BF. To test this hypothesis, we measured changes in the excitatory postsynaptic currents in pyramidal neurons of layer III/IV in the auditory cortex following high-frequency stimulation (HFS) of the MGBv, using whole cell recordings in an auditory thalamocortical slice. Our data showed that in response to the HFS of the MGBv the excitatory postsynaptic currents of AC neurons showed long-term bidirectional synaptic plasticity and long-term potentiation and depression. Pharmacological studies indicated that the long-term synaptic plasticity was induced through the activation of different sets of N-methyl-d-aspartate-type glutamatergic receptors, γ-aminobutyric acid-type receptors, and type 5 metabotropic glutamate receptors. Our data further demonstrated that blocking of different receptors with specific antagonists significantly inhibited MGBv stimulation-induced long-term plasticity as well as the shift of BF. These data indicate that these receptors have an important role in mediating frequency-specific auditory cortical plasticity.
电刺激内侧膝状体腹侧部（MGBv）神经元会引起听觉皮层（AC）神经元的频率调谐曲线向刺激的 MGBv 神经元的最佳频率（BF）转移（频率特异性可塑性）。BF 的转移是通过抑制记录的 AC 神经元的 BF 反应引起的，同时刺激的 MGBv 神经元的 BF 反应得到促进。然而，突触机制尚不清楚。我们假设，丘脑皮质突触传递和受体功能的激活可能有助于 MGBv 刺激诱导的频率特异性听觉可塑性和 BF 的转移。为了验证这一假设，我们使用听觉丘脑皮质切片中的全细胞膜片记录，测量了 MGBv 高频刺激（HFS）后 III/IV 层锥体神经元的兴奋性突触后电流的变化。我们的数据表明，MGBv 的 HFS 会引起 AC 神经元的兴奋性突触后电流产生长期双向突触可塑性，表现为长时程增强和长时程抑制。药理学研究表明，这种长期突触可塑性是通过激活不同的 N-甲基-D-天冬氨酸型谷氨酸能受体、γ-氨基丁酸型受体和 5 型代谢型谷氨酸受体来诱导的。我们的数据进一步表明，用特定的拮抗剂阻断不同的受体，显著抑制了 MGBv 刺激诱导的长期可塑性以及 BF 的转移。这些数据表明，这些受体在介导频率特异性听觉皮质可塑性方面具有重要作用。
