Ablation of C-fibers decreases quantal size of GABAergic synaptic transmission in the insular cortex.

Ablation of C-fibers decreases quantal size of GABAergic synaptic transmission in the insular cortex.
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C 纤维的消融降低了岛叶皮质中 GABA 能突触传递的量子大小。

DOI:
10.1016/j.neuroscience.2017.09.052
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发表时间:
2017
期刊:
影响因子:
3.3
通讯作者:
Kobayashi M
Kobayashi M
中科院分区:
医学3区
文献类型:
--
作者:
Murayama S;Yamamoto K;Kaneko M;Ogiso B;Kobayashi M

文献摘要

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初级感觉皮层对感觉障碍表现出神经可塑性变化,GABA能突触传递在可塑性调节中起着关键作用。岛叶皮层(IC)整合通过有髓Aδ-和无髓C-纤维传递的口面伤害性信号。然而,它一直是未知的伤害性输入的干扰,如周围神经的删除,改变GABA能局部电路IC。本研究在出生后1- 2d注射辣椒素(capsaicin)切除大鼠C纤维的模型中,阐明了GABA能突触传递,在体光学成像显示辣椒素处理的大鼠对牙髓刺激的IC表现出易化兴奋性传播。全细胞膜片钳技术记录的锥体神经元(Pyr)显示,辣椒素处理组大鼠的微小抑制性突触后电流(IPSCs)的幅度较假处理组小,但频率无明显变化。此外,细胞外Ca 2+的替代Sr 2+,这会导致在量子尺寸的神经递质的异步释放,诱导辣椒素处理的大鼠中从快速尖峰的GABA能中间神经元到Pyr连接记录的异步单一IPSC的幅度比假处理的大鼠小。这些结果表明辣椒素处理通过突触后机制抑制IPSC。为了证实这种可能性,采用方差-均值分析的单一IPSC,我们发现,GABA能突触传递的量子尺寸在辣椒素治疗的大鼠比假治疗的大鼠更小。这些结果表明,C纤维的消融引起GABA能突触传递的可塑性变化,通过减少突触后GABA A受体介导的电导,这是辣椒素处理的大鼠IC易化兴奋的可能机制。
The primary sensory cortex exhibits neuroplastic changes responding to sensory disturbances, and GABAergic synaptic transmission plays a critical role in the regulation of plasticity. The insular cortex (IC) integrates orofacial nociceptive signals conveyed via myelinated Aδ- and unmyelinated C-fibers. However, it has been unknown whether a disturbance of nociceptive inputs, such as a deletion of the peripheral nerves, alters GABAergic local circuit in IC. The present study elucidated GABAergic synaptic transmission in the model rat whose C-fibers were ablated by capsaicin injection 1–2 days after birth.In vivooptical imaging revealed that capsaicin-treated rats showed a facilitative excitatory propagation in IC responding to dental pulp stimulation. Whole-cell patch-clamp recording from pyramidal neurons (Pyr) demonstrated that capsaicin-treated rats showed the smaller amplitude of miniature inhibitory postsynaptic currents (IPSCs) than sham-treated rats without changing the frequency. Furthermore, replacement of extracellular Ca2+to Sr2+, which induces an asynchronous release of neurotransmitters in the quantal size, induced a smaller amplitude of asynchronous unitary IPSCs recorded from fast-spiking GABAergic interneuron to Pyr connections in capsaicin-treated rats than sham-treated rats. These results suggest that capsaicin treatment depresses IPSCs via a postsynaptic mechanism. To confirm this possibility, the variance-mean analysis of unitary IPSCs was employed and we found that quantal size of GABAergic synaptic transmission was smaller in capsaicin-treated rats than in sham-treated rats. These results suggest that ablation of C-fibers induces plastic changes in GABAergic synaptic transmission by decreasing postsynaptic GABAAreceptor-mediated conductance, which is a possible mechanism of the facilitative excitation in IC of capsaicin-treated rats.