Presynaptic GABAB receptors modulate thalamic excitation of inhibitory and excitatory neurons in the mouse barrel cortex
Presynaptic GABAB receptors modulate thalamic excitation of inhibitory and excitatory neurons in the mouse barrel cortex
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DOI：
10.1152/jn.00196.2004
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发表时间：
2004-11-01
影响因子：
2.5
通讯作者：
Nieves, D
中科院分区：
文献类型：
--
作者：
Porter, JT;Nieves, D
皮质抑制在感觉信息加工中起着重要作用，体内应用GABA(B)受体拮抗剂扩大感受野表明GABA(B)受体介导了部分皮质抑制。虽然有证据表明皮质神经元上存在突触后GABA(B)受体，但丘脑皮质末梢上没有GABA(B)受体。因此，为了确定突触前GABA(B)受体是否调节小鼠体感“桶”皮层第IV层抑制性神经元和第II-III和第IV层兴奋性神经元的丘脑兴奋，我们使用了丘脑皮层切片制备和膜片钳电生理。腹基底丘脑的刺激引起皮层神经元的兴奋性突触后电流（EPSCs）。巴氯芬是一种选择性GABA(B)受体激动剂，可使抑制性和兴奋性神经元中AMPA受体介导的和n -甲基- d -天冬氨酸（NMDA）受体介导的epsc可逆地减少。GABA(B)受体拮抗剂CGP 35348逆转了巴氯芬产生的抑制作用。以Cs+为基础的记录溶液阻断突触后GABA(B)受体介导的作用不影响抑制作用，表明巴氯芬具有突触前作用。巴氯芬可逆地增加配对脉冲比和变异系数，与突触前抑制谷氨酸释放一致。我们的研究结果表明，GABA(B)受体的突触前激活调节了抑制性和兴奋性神经元的丘脑皮质兴奋，并提供了皮层抑制调节感觉信息加工的另一种机制。
Cortical inhibition plays an important role in the processing of sensory information, and the enlargement of receptive fields by the in vivo application of GABA(B) receptor antagonists indicates that GABA(B) receptors mediate some of this cortical inhibition. Although there is evidence of postsynaptic GABA(B) receptors on cortical neurons, there is no evidence of GABA(B) receptors on thalamocortical terminals. Therefore to determine if presynaptic GABA(B) receptors modulate the thalamic excitation of layer IV inhibitory neurons and excitatory neurons in layers II-III and IV of the somatosensory "barrel" cortex of mice, we used a thalamocortical slice preparation and patch-clamp electrophysiology. Stimulation of the ventrobasal thalamus elicited excitatory postsynaptic currents (EPSCs) in cortical neurons. Bath application of baclofen, a selective GABA(B) receptor agonist, reversibly decreased AMPA receptor-mediated and N-methyl-D-aspartate(NMDA) receptor-mediated EPSCs in inhibitory and excitatory neurons. The GABA(B) receptor antagonist, CGP 35348, reversed the inhibition produced by baclofen. Blocking the postsynaptic GABA(B) receptor-mediated effects with a Cs+-based recording solution did not affect the inhibition, suggesting a presynaptic effect of baclofen. Baclofen reversibly increased the paired-pulse ratio and the coefficient of variation, consistent with the presynaptic inhibition of glutamate release. Our results indicate that the presynaptic activation of GABA(B) receptors modulates thalamocortical excitation of inhibitory and excitatory neurons and provide another mechanism by which cortical inhibition can modulate the processing of sensory information.