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首页> 外文期刊>The European Journal of Neuroscience >Two differential frequency-dependent mechanisms regulating tonic firing of thalamic reticular neurons.
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Two differential frequency-dependent mechanisms regulating tonic firing of thalamic reticular neurons.

机译：两种不同的频率依赖性机制调节丘脑网状神经元的强直性放电。

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Transmission through the thalamus activates circuits involving the GABAergic neurons of the thalamic reticular nucleus (TRN). TRN cells receive excitatory inputs from thalamocortical and corticothalamic cells and send inhibitory projections to thalamocortical cells. The inhibitory output of TRN neurons largely depends on the level of excitatory drive to these cells but may also be partly under the control of mechanisms intrinsic to the TRN. We examined two such possible mechanisms, short-term plasticity at glutamatergic synapses in the TRN and intra-TRN inhibition. In rat brain slices, responses of TRN neurons to brief trains of stimuli applied to glutamatergic inputs were recorded in voltage- or current-clamp mode. In voltage clamp, TRN cells showed no change in alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated excitatory postsynaptic current amplitudes to stimulation at non-gamma frequencies (< 30 Hz), simulating background activity, but exhibited short-term depressionin these amplitudes to stimulation at gamma frequencies (> 30 Hz), simulating sensory transmission. In current clamp, TRN cells increased their spike outputs in burst and tonic firing modes to increasing stimulus-train frequencies. These increases in spike output were most likely due to temporal summation of excitatory postsynaptic potentials. However, the frequency-dependent increase in tonic firing was attenuated at gamma stimulus frequencies, indicating that the synaptic depression selectively observed in this frequency range acts to suppress TRN cell output. In contrast, intra-TRN inhibition reduced spike output selectively at non-gamma stimulus frequencies. Thus, our data indicate that two intrinsic mechanisms play a role in controlling the tonic spike output of TRN neurons and these mechanisms are differentially related to two physiologically meaningful stimulus frequency ranges.
机译：通过丘脑的传输激活了涉及丘脑网状核（TRN）的GABA能神经元的回路。 TRN细胞接受来自丘脑皮质和皮质丘脑细胞的兴奋性输入，并向丘脑皮质细胞发送抑制性投射。 TRN神经元的抑制性输出很大程度上取决于对这些细胞的兴奋性驱动水平，但也可能部分受TRN固有机制的控制。我们研究了两种可能的机制，即TRN中的谷氨酸能突触的短期可塑性和TRN内的抑制。在大鼠脑切片中，以电压或电流钳模式记录了TRN神经元对施加于谷氨酸能输入的简短刺激序列的反应。在电压钳中，TRN细胞在非γ频率（<30 Hz）下对刺激的突触后突触后电流幅值没有变化，这是由α-氨基-3-羟基-5-羟基-5-甲基异恶唑-4-丙酸（AMPA）受体介导的。本底活动，但在这些振幅上表现出短期抑制作用，以在伽马频率（> 30 Hz）下刺激，模拟了感觉传递。在电流钳中，TRN细胞以爆发和强音发射模式增加其尖峰输出，以增加刺激训练频率。峰值输出的增加很可能是由于兴奋性突触后电位的时间总和。但是，在伽马刺激频率下，频率依赖性的强直性发声的增加减弱了，这表明在该频率范围内选择性观察到的突触抑制作用抑制了TRN细胞的输出。相反，TRN内抑制在非伽马刺激频率下选择性降低了尖峰输出。因此，我们的数据表明，两个内在机制在控制TRN神经元的补品尖峰输出中发挥作用，并且这些机制与两个生理学上有意义的刺激频率范围存在差异。

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