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Photobiomodulation-induced changes in a monkey model of Parkinson's disease: changes in tyrosine hydroxylase cells and GDNF expression in the striatum.

Identifieur interne : 004481 ( Ncbi/Merge ); précédent : 004480; suivant : 004482

Photobiomodulation-induced changes in a monkey model of Parkinson's disease: changes in tyrosine hydroxylase cells and GDNF expression in the striatum.

Auteurs : Nabil El Massri [Australie] ; Ana P. Lemgruber [Australie] ; Isobel J. Rowe [Australie] ; Cécile Moro [France] ; Napoleon Torres [France] ; Florian Reinhart [France] ; Claude Chabrol [France] ; Alim-Louis Benabid [France] ; John Mitrofanis [Australie]

Source :

RBID : pubmed:28299414

Abstract

Intracranial application of red to infrared light, known also as photobiomodulation (PBM), has been shown to improve locomotor activity and to neuroprotect midbrain dopaminergic cells in rodent and monkey models of Parkinson's disease. In this study, we explored whether PBM has any influence on the number of tyrosine hydroxylase (TH)(+)cells and the expression of GDNF (glial-derived neurotrophic factor) in the striatum. Striatal sections of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-treated mice and monkeys and 6-hydroxydopamine (6OHDA)-lesioned rats that had PBM optical fibres implanted intracranially (or not) were processed for immunohistochemistry (all species) or western blot analysis (monkeys). In our MPTP monkey model, which showed a clear loss in striatal dopaminergic terminations, PBM generated a striking increase in striatal TH(+) cell number, 60% higher compared to MPTP monkeys not treated with PBM and 80% higher than controls. This increase was not evident in our MPTP mouse and 6OHDA rat models, both of which showed minimal loss in striatal terminations. In monkeys, the increase in striatal TH(+) cell number in MPTP-PBM cases was accompanied by similar increases in GDNF expression, as determined from western blots, from MPTP and control cases. In summary, these results offer insights into the mechanisms by which PBM generates its beneficial effects, potentially with the use of trophic factors, such as GDNF.

DOI: 10.1007/s00221-017-4937-0
PubMed: 28299414

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pubmed:28299414

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<div type="abstract" xml:lang="en">Intracranial application of red to infrared light, known also as photobiomodulation (PBM), has been shown to improve locomotor activity and to neuroprotect midbrain dopaminergic cells in rodent and monkey models of Parkinson's disease. In this study, we explored whether PBM has any influence on the number of tyrosine hydroxylase (TH)(+)cells and the expression of GDNF (glial-derived neurotrophic factor) in the striatum. Striatal sections of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-treated mice and monkeys and 6-hydroxydopamine (6OHDA)-lesioned rats that had PBM optical fibres implanted intracranially (or not) were processed for immunohistochemistry (all species) or western blot analysis (monkeys). In our MPTP monkey model, which showed a clear loss in striatal dopaminergic terminations, PBM generated a striking increase in striatal TH(+) cell number, 60% higher compared to MPTP monkeys not treated with PBM and 80% higher than controls. This increase was not evident in our MPTP mouse and 6OHDA rat models, both of which showed minimal loss in striatal terminations. In monkeys, the increase in striatal TH(+) cell number in MPTP-PBM cases was accompanied by similar increases in GDNF expression, as determined from western blots, from MPTP and control cases. In summary, these results offer insights into the mechanisms by which PBM generates its beneficial effects, potentially with the use of trophic factors, such as GDNF.</div>
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<RefSource>Ann Neurol. 2016 Jan;79(1):59-75</RefSource>
<PMID Version="1">26456231</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites">
<RefSource>Parkinsonism Relat Disord. 2012 Jun;18(5):469-76</RefSource>
<PMID Version="1">22285756</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites">
<RefSource>Front Neuroanat. 2015 Feb 13;9:10</RefSource>
<PMID Version="1">25762899</PMID>
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<CommentsCorrections RefType="Cites">
<RefSource>Brain Struct Funct. 2015 Jan;220(1):331-49</RefSource>
<PMID Version="1">24173616</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="Cites">
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