Neurotransmitter release changes induced by low power 830 nm diode laser irradiation on the neuromuscular junctions of the mouse.

BACKGROUND AND OBJECTIVE: Treating patients with a Gallium-Aluminum-Arsenide (GaAlAs) infrared (IR) diode laser reduces muscle spasm and increases mobility in the muscles. The effect of low intensity laser irradiation on nerve function, growth, and repair mechanisms is a contentious area of research. We have addressed one aspect of this controversy by systematically examining the influence of 830 nm laser radiation on neurotransmitter release in neuromuscular junctions (NMJ) of the mouse diaphragm. STUDY DESIGN/MATERIALS AND METHODS: Thirty adult mice were studied. Diode laser GaAlAs 830 nm (4 and 12 J/cm2) was used. Neurotransmitter release was studied by conventional intracellular recording techniques on curarized muscles or high magnesium media. The quantal content, amplitude, and latency of the end-plate potentials (EPPs) were analyzed. Frequency and amplitude were evaluated for the miniature end-plate potentials (MEPPs). Facilitation of the neurotransmitter release was also evaluated by paired pulse stimulation. RESULTS AND CONCLUSIONS: The irradiated (12 J/cm2) muscles showed a significant reduction in quantal content (P = 0.01) and EPP amplitude (P = 0.04), but the latency, spontaneous transmitter release (MEPPs) and paired pulse facilitation did not change. No alterations were observed in NMJ irradiated with 4 J/cm2. We conclude that 830 nm diode laser irradiation (at a dose of 12 J/cm2) can affect the evoked neurotransmitter release in the mouse motor endplates.

Effect of low power 655 nm diode laser irradiation on the neuromuscular junctions of the mouse diaphragm.

BACKGROUND AND OBJECTIVES: Low level laser therapy (LLLT) in specific wavelengths and fluence maintains the electrophysiological activity of injured peripheral nerve in rats, preventing scar formation (at injury site) as well as degenerative changes in the corresponding motor neurons of the spinal cord, thus accelerating regeneration of the injured nerve. We studied the effect of LLLT on the neurotransmitter release in neuromuscular junctions of the mouse diaphragm. STUDY DESIGN/MATERIALS AND METHODS: Thirty-nine diaphragm muscles were studied. LLLT with GaAlAs 655 nm (1-12 J/cm(2)) was used. Neurotransmitter release was studied by conventional intracellular recording techniques on curarised or high magnesium media. Quantal content, amplitude, latency and rise time were analysed for end-plate potentials (EPPs). Frequency and amplitude were evaluated for the miniature end-plate potentials (MEPPs). Short-term plasticity of the neurotransmitter release (fast facilitation) was also evaluated by paired pulse stimulation. RESULTS AND CONCLUSIONS: This study showed that LLLT (655 nm) in these doses has no detectable physiological effect on the motor end-plate neurotransmitter release in mice.

Effect of low-power GaAlAs laser (660 nm) on bone structure and cell activity: an experimental animal study.

Low-level laser therapy (LLLT) is increasingly being used in the regeneration of soft tissue. In the regeneration of hard tissue, it has already been shown that the biomodulation effect of lasers repairs bones more quickly. We studied the activity in bone cells after LLLT close to the site of the bone injury. The femurs of 48 rats were perforated (24 in the irradiated group and 24 in the control group) and the irradiated group was treated with a GaAlAs laser of 660 nm, 10 J/cm2 of radiant exposure on the 2nd, 4th, 6th and 8th days after surgery (DAS). We carried out histomorphometry analysis of the bone. We found that activity was higher in the irradiated group than in the control group: (a) bone volume at 5 DAS (p=0.035); (b) osteoblast surface at 15 DAS (p=0.0002); (c) mineral apposition rate at 15 and 25 DAS (p=0.0008 and 0.006); (d) osteoclast surface at 5 DAS and 25 DAS (p=0.049 and p=0.0028); and (e) eroded surface ( p=0.0032). We concluded that LLLT increases the activity in bone cells (resorption and formation) around the site of the repair without changing the bone structure.