830 nm laser irradiation induces varicosity formation, reduces mitochondrial membrane potential and blocks fast axonal flow in small and medium diameter rat dorsal root ganglion neurons: implications for the analgesic effects of 830 nm laser

Authors

  • Roberta T Chow,

    Corresponding author
    1. 1 Castle Hill Medical Centre, Private Medical Practice; 2Discipline of Medicine and; 3Nerve Research Foundation, The University of Sydney, Sydney, Australia
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  • 1,2 Monique A David,

    1. 1 Castle Hill Medical Centre, Private Medical Practice; 2Discipline of Medicine and; 3Nerve Research Foundation, The University of Sydney, Sydney, Australia
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  • and 2 Patricia J Armati 3

    1. 1 Castle Hill Medical Centre, Private Medical Practice; 2Discipline of Medicine and; 3Nerve Research Foundation, The University of Sydney, Sydney, Australia
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Dr. Roberta T. Chow, MB BS (Hons), FRACGP, FAMAC, MApplSci (Med Acu), Nerve Research Foundation, Room 475, Blackburn Building, D06, The University of Sydney, NSW 2006, Australia. E-mail: rtchow@bigpond.net.au

Abstract

Abstract  We report the formation of 830 nm (cw) laser-induced, reversible axonal varicosities, using immunostaining with β-tubulin, in small and medium diameter, TRPV-1 positive, cultured rat DRG neurons. Laser also induced a progressive and statistically significant decrease (p < 0.005) in MMP in mitochondria in and between static axonal varicosities. In cell bodies of the neuron, the decrease in MMP was also statistically significant (p < 0.05), but the decrease occurred more slowly. Importantly we also report for the first time that 830 nm (cw) laser blocked fast axonal flow, imaged in real time using confocal laser microscopy and JC-1 as mitotracker.

Control neurons in parallel cultures remained unaffected with no varicosity formation and no change in MMP. Mitochondrial movement was continuous and measured along the axons at a rate of 0.8 μm/s (range 0.5–2 μm/s), consistent with fast axonal flow. Photoacceptors in the mitochondrial membrane absorb laser and mediate the transduction of laser energy into electrochemical changes, initiating a secondary cascade of intracellular events. In neurons, this results in a decrease in MMP with a concurrent decrease in available ATP required for nerve function, including maintenance of microtubules and molecular motors, dyneins and kinesins, responsible for fast axonal flow. Laser-induced neural blockade is a consequence of such changes and provide a mechanism for a neural basis of laser-induced pain relief. The repeated application of laser in a clinical setting modulates nociception and reduces pain. The application of laser therapy for chronic pain may provide a non-drug alternative for the management of chronic pain.

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