Abstract
We examined whether near-infrared light (NIr) treatment (photobiomodulation) saves dopaminergic amacrine cells of the retina in an acute and a chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson disease. For the acute model, BALB/c mice had MPTP (100 mg/kg) or saline injections over 30 hours, followed by a six-day-survival period. For the chronic model, mice had MPTP (200 mg/kg) or saline injections over five weeks, followed by a three-week-survival period. NIr treatment was applied either at the same time (simultaneous series) or well after (posttreatment series) the MPTP insult. There were four groups within each series: Saline, Saline-NIr, MPTP, and MPTP-NIr. Retinae were processed for tyrosine hydroxylase (TH) immunochemistry, and cell number was analysed. In the MPTP groups, there was a significant reduction in TH+ cell number compared to the saline controls; this reduction was greater in the acute (~50%) compared to the chronic (~30%) cases. In the MPTP-NIr groups, there were significantly more TH+ cells than in the MPTP groups of both series (~30%). In summary, we showed that NIr treatment was able to both protect (simultaneous series) and rescue (posttreatment series) TH+ cells of the retina from parkinsonian insult.
Highlights
Many previous studies have reported that mitochondrial dysfunction is a key component of the pathogenesis of Parkinson disease, a striking motor disorder that develops after a major loss of dopaminergic cells in the substantia nigra pars compacta (SNc) [1]
We sought to extend our previous findings on the SNc of MPTP-treated mice [4, 5] by exploring whether near infrared light (NIr) treatment enhances the survival of tyrosine hydroxylase (TH)+ dopaminergic cells located in the retina
Confirming previous studies [10, 19, 20], TH immunoreactivity in the mouse retina was seen in amacrine cells with large oval- or triangular-shaped somata (Figure 1(c)) located mainly in the inner part of the inner nuclear layer (Figure 1(d)); only one or two cells per retina were ever seen in the ganglion cell layer (Figure 1(e))
Summary
Many previous studies have reported that mitochondrial dysfunction is a key component of the pathogenesis of Parkinson disease, a striking motor disorder that develops after a major loss of dopaminergic cells in the substantia nigra pars compacta (SNc) [1]. Treatments that target the protection and/or enhancement of mitochondrial function against insult may prove to be useful therapeutic tools. One such treatment is low intensity light therapy, known as photobiomodulation or near infrared light (NIr) treatment. Previous studies have shown that when exposing cells to NIr treatment, mitochondrial function and ATP (adenosine5 -triphosphate) synthesis are enhanced considerably [2, 3]. We sought to extend our previous findings on the SNc of MPTP-treated mice [4, 5] by exploring whether NIr treatment enhances the survival of tyrosine hydroxylase (TH)+ dopaminergic cells located in the retina. ISRN Neurology for this study were from the same animals as those used in previous acute [4] and chronic [5] MPTP studies exploring the number of TH+ cells in the SNc
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