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A Protocol for Transcranial Photobiomodulation Therapy in Mice
Published on: November 18, 2018
Low-level laser therapy (810 nm) protects primary cortical neurons against excitotoxicity in vitro
Ying-Ying Huang1, Kazuya Nagata, Clark E Tedford
1Wellman Center for Photomedicine, Massachusetts General Hospital, 40 Blossom Street, Boston MA 02114, USA; Department of Dermatology, Harvard Medical School, Boston MA, USA; Department of Pathology, Guangxi Medical University, Nanning, Guangxi, China.
Abstract:
Excitotoxicity describes a pathogenic process whereby death of neurons releases large amounts of the excitatory neurotransmitter glutamate, which then proceeds to activate a set of glutamatergic receptors on neighboring neurons (glutamate, N-methyl-D-aspartate (NMDA), and kainate), opening ion channels leading to an influx of calcium ions producing mitochondrial dysfunction and cell death. Excitotoxicity contributes to brain damage after stroke, traumatic brain injury, and neurodegenerative diseases, and is also involved in spinal cord injury. We tested whether low level laser (light) therapy (LLLT) at 810 nm could protect primary murine cultured cortical neurons against excitotoxicity in vitro produced by addition of glutamate, NMDA or kainate. Although the prevention of cell death was modest but significant, LLLT (3 J/cm(2) delivered at 25 mW/cm(2) over 2 min) gave highly significant benefits in increasing ATP, raising mitochondrial membrane potential, reducing intracellular calcium concentrations, reducing oxidative stress and reducing nitric oxide. The action of LLLT in abrogating excitotoxicity may play a role in explaining its beneficial effects in diverse central nervous system pathologies.
Insights
Low level laser therapy (LLLT) shows promise in protecting neurons from excitotoxicity, a process involved in brain injury and neurodegenerative diseases. This therapy significantly improved cellular energy, mitochondrial function, and reduced damaging calcium and oxidative stress in neurons.
Area of Science:
- Neuroscience
- Cell Biology
- Biomedical Engineering
Background:
- Excitotoxicity is a neuronal death pathway involving glutamate receptor overactivation and calcium influx.
- This process contributes to neuronal damage in stroke, traumatic brain injury, and neurodegenerative diseases.
- Understanding protective mechanisms against excitotoxicity is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the neuroprotective effects of 810 nm low-level laser therapy (LLLT) against excitotoxicity in primary cortical neurons.
- To determine if LLLT can mitigate cell death induced by glutamate, N-methyl-D-aspartate (NMDA), or kainate.
Main Methods:
- Primary murine cortical neurons were cultured in vitro.
- Excitotoxicity was induced by adding glutamate, NMDA, or kainate.
- Neurons were treated with 810 nm LLLT (3 J/cm(2) at 25 mW/cm(2) for 2 min).
- Cell viability, ATP levels, mitochondrial membrane potential, intracellular calcium, oxidative stress, and nitric oxide were assessed.
Main Results:
- LLLT demonstrated a modest but significant prevention of neuronal cell death.
- LLLT significantly increased ATP production and mitochondrial membrane potential.
- LLLT effectively reduced intracellular calcium concentrations, oxidative stress, and nitric oxide levels.
Conclusions:
- LLLT exhibits neuroprotective properties against excitotoxicity in vitro.
- The observed benefits of LLLT include improved cellular energy metabolism and reduced markers of cellular damage.
- LLLT's ability to abrogate excitotoxicity may contribute to its therapeutic potential in central nervous system disorders.
