Influence of gap junctions upon Ca2+ propagation from stimulated keratinocytes to DRG neurons.

Biophysics and Physicobiology Pub Date : 2022-09-22 eCollection Date: 2022-01-01 DOI:10.2142/biophysico.bppb-v19.0041
Chiaki Seto, Kenta Toyoda, Kousuke Inada, Kotaro Oka, Etsuro Ito
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Abstract

Epidermal cells, such as keratinocytes, are regarded as the first sensory cells to transmit nociception and mechanoreception to free nerve endings extended from the dorsal root ganglion (DRG). Previous studies suggested that this transmission occurs as Ca2+ propagation via ATP receptors. Conversely, the influence of gap junctions on this Ca2+ propagation is largely unknown. Thus, we examined the localization and the role of connexin 43 among keratinocytes and DRG neurons. We co-cultured keratinocytes and DRG neurons and investigated the effect of pharmacological blockade of gap junctions on Ca2+ propagation upon stimulation of a single keratinocyte. Immunocytochemical experiments showed that connexin 43 is localized between keratinocytes and between keratinocytes and DRG neurons. Octanol, a gap junction inhibitor, significantly suppressed the concentrical Ca2+ propagation. Therefore, we conclude that the Ca2+ propagation mechanism via gap junctions from stimulated keratinocytes to free nerve endings should be taken into account.

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间隙连接对Ca2+从受刺激的角质形成细胞向DRG神经元传播的影响。
表皮细胞,如角化细胞,被认为是最早将伤害感受和机械感受传递到从背根神经节(DRG)延伸出来的自由神经末梢的感觉细胞。先前的研究表明,这种传递是通过ATP受体的Ca2+传播发生的。相反,间隙连接对Ca2+传播的影响在很大程度上是未知的。因此,我们研究了连接蛋白43在角化细胞和DRG神经元中的定位和作用。我们共培养角质形成细胞和DRG神经元,并研究了在刺激单个角质形成细胞时,药物阻断间隙连接对Ca2+增殖的影响。免疫细胞化学实验表明,连接蛋白43定位于角化细胞之间以及角化细胞与DRG神经元之间。辛醇是一种间隙连接抑制剂,可以显著抑制Ca2+的同心增殖。因此,我们得出结论,Ca2+通过间隙连接从刺激角质形成细胞到自由神经末梢的传播机制应该被考虑在内。
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