Hin Heng Lo, Tawan Munkongcharoen, Rosa M Muijen, Ritika Gurung, Anjali G Umredkar, Mark D Baker
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引用次数: 0
摘要
红外线激光照射视神经轴突时,其电流阈值会升高,但人们对其机理仅有部分了解。在离体大鼠视神经中,通过柔性光纤在电刺激部位附近施加激光。在持续 3 分钟的单次激光照射中,阈值迅速升高,随后逐渐减弱,其时间常数在 40 至 50 秒之间。38.6 mM Li+与 5 μ M 布美他尼联合使用可部分阻断阈值的增加,这种方法可增加折射性,与轴突去极化一致。通过评估激光对神经输入电阻的影响,排除了之前提出的髓鞘电阻下降导致阈值变化的可能性。这些数据似乎与轴突膜电位部分依赖于温度依赖性电中性Na+流入一致,对激光的反应减弱可能是由于细胞内[Na+]下降,Na+泵诱导的超极化逐渐减弱所致。
Application of near infra-red laser light increases current threshold in optic nerve consistent with increased Na+-dependent transport.
Increases in the current threshold occur in optic nerve axons with the application of infra-red laser light, whose mechanism is only partly understood. In isolated rat optic nerve, laser light was applied near the site of electrical stimulation, via a flexible fibre optic. Paired applications of light produced increases in threshold that were reduced on the second application, the response recovering with increasing delays, with a time constant of 24 s. 3-min duration single applications of laser light gave rise to a rapid increase in threshold followed by a fade, whose time-constant was between 40 and 50 s. After-effects were sometimes apparent following the light application, where the resting threshold was reduced. The increase in threshold was partially blocked by 38.6 mM Li+ in combination with 5 M bumetanide, a manoeuvre increasing refractoriness and consistent with axonal depolarization. Assessing the effect of laser light on the nerve input resistance ruled out a previously suggested fall in myelin resistance as contributing to threshold changes. These data appear consistent with an axonal membrane potential that partly relies on temperature-dependent electroneutral Na+ influx, and where fade in the response to the laser may be caused by a gradually diminishing Na+ pump-induced hyperpolarization, in response to falling intracellular [Na+].
期刊介绍:
Pflügers Archiv European Journal of Physiology publishes those results of original research that are seen as advancing the physiological sciences, especially those providing mechanistic insights into physiological functions at the molecular and cellular level, and clearly conveying a physiological message. Submissions are encouraged that deal with the evaluation of molecular and cellular mechanisms of disease, ideally resulting in translational research. Purely descriptive papers covering applied physiology or clinical papers will be excluded. Papers on methodological topics will be considered if they contribute to the development of novel tools for further investigation of (patho)physiological mechanisms.