U-1051, INSERM Institut des Neurosciences de Montpellier, Montpellier, France.
J Neurophysiol. 2012 Jun;107(12):3227-34. doi: 10.1152/jn.00424.2011. Epub 2012 Mar 21.
Infrared laser irradiation has been established as an appropriate stimulus for primary sensory neurons under conditions where sensory receptor cells are impaired or lost. Yet, development of clinical applications has been impeded by lack of information about the molecular mechanisms underlying the laser-induced neural response. Here, we directly address this question through pharmacological characterization of the biological response evoked by midinfrared irradiation of isolated retinal and vestibular ganglion cells from rodents. Whole cell patch-clamp recordings reveal that both voltage-gated calcium and sodium channels contribute to the laser-evoked neuronal voltage variations (LEVV). In addition, selective blockade of the LEVV by micromolar concentrations of ruthenium red and RN 1734 identifies thermosensitive transient receptor potential vanilloid channels as the primary effectors of the chain reaction triggered by midinfrared laser irradiation. These results have the potential to facilitate greatly the design of future prosthetic devices aimed at restoring neurosensory capacities in disabled patients.
红外激光辐射已被确立为一种适当的刺激物，适用于在感觉感受器细胞受损或丧失的情况下的初级感觉神经元。然而，由于缺乏关于激光诱导神经反应的分子机制的信息，临床应用的发展受到了阻碍。在这里，我们通过对来自啮齿动物的分离视网膜和前庭神经节细胞的中红外辐射的生物学反应进行药理学表征，直接解决了这个问题。全细胞膜片钳记录显示，电压门控钙和钠通道都有助于激光诱发的神经元电压变化（LEVV）。此外，通过微摩尔浓度的钌红和 RN 1734 选择性阻断 LEVV，鉴定出热敏瞬时受体电位香草素通道作为中红外激光辐射触发的连锁反应的主要效应器。这些结果有可能极大地促进未来旨在恢复残疾患者神经感觉能力的假体设备的设计。
