Near‐infrared laser photons induce glutamate release from cerebrocortical nerve terminals

Amaroli, Andrea; Marcoli, Manuela; Venturini, Arianna; Passalacqua, Mario; Agnati, Luigi F.; Signore, Antonio; Raffetto, Mirco; Maura, Guido; Benedicenti, Stefano; Cervetto, Chiara

doi:10.1002/jbio.201800102

Cited by 23 publications

(24 citation statements)

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“…Calcium may have also a role in this issue. Indeed, de Freitas Rodrigues [ 34 ] and Pigatto et al [ 110 ] showed that PBM decreased TRPV1 expression, and Amaroli et al [ 111 ] demonstrated that 808-nm laser light induced calcium-dependent glutamate release from nerve terminals, only in the presence of mitochondria. It is known that glutamate release is associated with ATP [ 112 ].…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial Bioenergetic, Photobiomodulation and Trigeminal Branches Nerve Damage, What’s the Connection? A Review

Ravera

Colombo

Pasquale

et al. 2021

IJMS

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Background: Injury of the trigeminal nerve in oral and maxillofacial surgery can occur. Schwann cell mitochondria are regulators in the development, maintenance and regeneration of peripheral nerve axons. Evidence shows that after the nerve injury, mitochondrial bioenergetic dysfunction occurs and is associated with pain, neuropathy and nerve regeneration deficit. A challenge for research is to individuate new therapies able to normalise mitochondrial and energetic metabolism to aid nerve recovery after damage. Photobiomodulation therapy can be an interesting candidate, because it is a technique involving cell manipulation through the photonic energy of a non-ionising light source (visible and NIR light), which produces a nonthermal therapeutic effect on the stressed tissue. Methods: The review was based on the following questions: (1) Can photo-biomodulation by red and NIR light affect mitochondrial bioenergetics? (2) Can photobiomodulation support damage to the trigeminal nerve branches? (preclinical and clinical studies), and, if yes, (3) What is the best photobiomodulatory therapy for the recovery of the trigeminal nerve branches? The papers were searched using the PubMed, Scopus and Cochrane databases. This review followed the ARRIVE-2.0, PRISMA and Cochrane RoB-2 guidelines. Results and conclusions: The reliability of photobiomodulatory event strongly bases on biological and physical-chemical evidence. Its principal player is the mitochondrion, whether its cytochromes are directly involved as a photoacceptor or indirectly through a vibrational and energetic variation of bound water: water as the photoacceptor. The 808-nm and 100 J/cm2 (0.07 W; 2.5 W/cm2; pulsed 50 Hz; 27 J per point; 80 s) on rats and 800-nm and 0.2 W/cm2 (0.2 W; 12 J/cm2; 12 J per point; 60 s, CW) on humans resulted as trustworthy therapies, which could be supported by extensive studies.

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Section: Discussionmentioning

confidence: 99%

Mitochondrial Bioenergetic, Photobiomodulation and Trigeminal Branches Nerve Damage, What’s the Connection? A Review

Ravera

Colombo

Pasquale

et al. 2021

IJMS

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“…In fact, we previously showed the ability of 808 nm 1 W, 1 W/cm 2 and 60 J/cm 2 to modulate the calcium homeostasis affecting mitochondria bioenergy production [26,27], through the mitochondrial respiratory chain [23,25,55,56], cell metabolism [26,50], and inflammatory cell pathways [57], to promote cell proliferation [50,55,57], tissue regeneration [28,30,58], and release of neurotransmitters [59]. Lastly, the target of PBM therapy and the alteration of energy category genes in both moderate and severe BP could also explain why our PBM therapy was unsuccessful if performed more than 1 year after the onset of palsy.…”

Section: Discussionmentioning

confidence: 99%

Recovery from Idiopathic Facial Paralysis (Bell’s Palsy) Using Photobiomodulation in Patients Non-Responsive to Standard Treatment: A Case Series Study

et al. 2021

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Diminished facial movement and marked facial asymmetry can lead to a consistent psychological burden. Bell′s palsy (BP) is one of the most common causes of facial nerve illness, which comes with unilateral acute facial paresis. Nowadays, no clear guidelines for treating BP are available. We carried out a case series study to test the efficacy of photobiomodulation (PBM) therapy in patients with BP non-responsive to standard treatment. The study was experimentally performed at the Department of Surgical and Diagnostic Sciences, University of Genoa (Genoa, Italy), in accordance with case report guidelines. Patients were referred to our department by colleagues for evaluation to be included in the case series because no consistent improvement was observed at least 3 months from the diagnosis of BP. All the patients interrupted their pharmacological therapy before the initiation of PBM therapy. PBM therapy (808 nm, 1 W irradiated in continuous-wave for 60 s on spot-size 1 cm2; 1 W/cm2; 60 J/cm2; and 60 J) was administered every 2 days until complete resolution. Evaluation of the House-Brackmann scale was performed before and after treatments. Fourteen patients were screened as eligible for the study. Patients were Caucasians (36% females and 64% males) with a mean age ± standard deviation of 56.07 ± 15.21 years. Eleven patients out of 14, who experienced BP a maximum of 6 months, completely recovered through PBM. The three patients that did not show improvement were those who had experienced BP for years. PBM could be a supportive therapy for the management of BP in patients non-responsive to standard treatment. However, randomized controlled trials are necessary to sustain our encouraging results, exclude bias, and better explain the boundary between the time from diagnosis and the recovery of BP through PBM therapy.

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“…Gliosomes are a purified preparation of astrocyte processes containing vesicles loaded with gliotransmitter, competent for gliotransmitter secretion [ 9 , 19 ]. Synaptosomes are a purified preparation of nerve terminals, negligibly contaminated by astrocytic, microglial or oligodendroglial particles, competent for the release of neurotransmitters in response to different stimulations [ 20 , 24 , 25 ]. Gliosomes and synaptosomes were washed by centrifugation, and the pellets were resuspended in standard physiological medium buffered with HEPES or in loading buffer for the WB analysis.…”

Section: Methodsmentioning

confidence: 99%

“…In this regard, we investigated the function of isolated cerebrocortical nerve terminals (synaptosomes) and astrocyte processes (gliosomes) prepared from adult Dach-SMOX mice. Isolated synaptosomes indeed preserve the features of in situ nerve terminals, and reflect the behaviour of the presynaptic terminals in neuron–astrocyte networks [ 18 , 19 , 20 ], while gliosomes preserve the features and reflect the behaviour of the astrocyte processes in the networks [ 19 , 21 , 22 ]. In synaptosomes and gliosomes from Dach-SMOX and control mice, we assessed the PA content, the oxidative stress markers, and the influx of calcium in response to glutamate receptor activation.…”

Section: Introductionmentioning

confidence: 99%

Reactive Astrocytosis in a Mouse Model of Chronic Polyamine Catabolism Activation

et al. 2021

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Background: In the brain, polyamines are mainly synthesized in neurons, but preferentially accumulated in astrocytes, and are proposed to be involved in neurodegenerative/neuroinflammatory disorders and neuron injury. A transgenic mouse overexpressing spermine oxidase (SMOX, which specifically oxidizes spermine) in the neocortex neurons (Dach-SMOX mouse) was proved to be a model of increased susceptibility to excitotoxic injury. Methods: To investigate possible alterations in synapse functioning in Dach-SMOX mouse, both cerebrocortical nerve terminals (synaptosomes) and astrocytic processes (gliosomes) were analysed by assessing polyamine levels, ezrin and vimentin content, glutamate AMPA receptor activation, calcium influx, and catalase activity. Results: The main findings are as follows: (i) the presence of functional calcium-permeable AMPA receptors in synaptosomes from both control and Dach-SMOX mice, and in gliosomes from Dach-SMOX mice only; (ii) reduced content of spermine in gliosomes from Dach-SMOX mice; and (iii) down-regulation and up-regulation of catalase activity in synaptosomes and gliosomes, respectively, from Dach-SMOX mice. Conclusions: Chronic activation of SMOX in neurons leads to major changes in the astrocyte processes including reduced spermine levels, increased calcium influx through calcium-permeable AMPA receptors, and stimulation of catalase activity. Astrocytosis and the astrocyte process alterations, depending on chronic activation of polyamine catabolism, result in synapse dysregulation and neuronal suffering.

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Near‐infrared laser photons induce glutamate release from cerebrocortical nerve terminals

Cited by 23 publications

References 50 publications

Mitochondrial Bioenergetic, Photobiomodulation and Trigeminal Branches Nerve Damage, What’s the Connection? A Review

Mitochondrial Bioenergetic, Photobiomodulation and Trigeminal Branches Nerve Damage, What’s the Connection? A Review

Recovery from Idiopathic Facial Paralysis (Bell’s Palsy) Using Photobiomodulation in Patients Non-Responsive to Standard Treatment: A Case Series Study

Reactive Astrocytosis in a Mouse Model of Chronic Polyamine Catabolism Activation

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