Input specific LTD induction mechanisms of suprgranular pyramidal neurons in the auditory cortex

听觉皮层（AC）的锥体神经元接收来自内侧膝状体（MGB）和其他锥体神经元（锥体输入）的谷氨酸能输入。我们发现，NMDA受体拮抗剂（NMDARs） 50 μM APV和代谢性谷氨酸受体拮抗剂（mGluRs） 500 μM MGPG仅能部分抑制颗粒上层长期抑郁（LTD）的诱导。而在APV和MCPG的混合中未观察到LTD。我们假设LTD对谷氨酸受体的混合依赖可能归因于MGB输入和锥体输入的异质性。为了验证这一假设，我们调整了切片角度和其他记录条件，在正常切片上记录突触后电位，而在MGB病变大鼠的切片上不记录突触后电位。在这些实验中，MCPG单独抑制了LTD。对条件进行了调整，使MGB输入对场电位的贡献最小。在这些实验中，APV单独抑制了LTD的诱导。有趣的是，20 μM硝苯地平（l型Ca^<2+>通道阻滞剂）在MGB病变大鼠的切片中部分抑制了LTD的诱导，而在正常切片中则没有。这些发现表明，LTD的诱导需要激活MGB输入突触中的mGluRs和锥体输入突触中的NMDARs。

Pyramidal neurons in the auditory cortex (AC) receive glutamatergic inputs from the medial geniculate body (MGB inputs) and other pyramidal neurons (pyramidal inputs). We found that the induction of long-term depression (LTD) in supragranular layers was only partially suppressed by 50 μM APV, an antagonist of NMDA receptors (NMDARs), and 500 μM MGPG, an antagonist of metabotropic glutamate receptors (mGluRs). However, LTD was not observed in the mixture of APV and MCPG. We hypothesized that the mixed dependence of LTD on glutamate receptors could be attributed to the heterogeneity of MGB inputs and pyramidal inputs. To test this hypothesis, the angle of slicing and other recording conditions were adjusted so that postsynaptic potentials were recorded in normal slices, but not in the slices prepared from the rats with MGB lesion. In these experiments, LTD was suppressed by MCPG alone. The conditions were adjusted to minimize the contribution of MGB inputs in field potentials. In these experiments, the induction of LTD was suppressed by APV alone. Interestingly, the induction of LTD was partially suppressed by 20 μM nifedipine, a blocker of L-type Ca^<2+> channels, in the slices prepared from the rats with MGB lesions, but not in normal slices. These findings suggest that the induction of LTD requires activation of mGluRs in the synapses of MGB inputs and of NMDARs in the synapses of pyramidal inputs.