Photobiomodulation reduces gliosis in the basal ganglia of aged mice

This study explored the effects of long-term photobiomodulation (PBM) on the glial and neuronal organization in the striatum of aged mice. Mice aged 12 months were pretreated with PBM (670 nm) for 20 minutes per day, commencing at 5 months old and continued for 8 months. We had 2 control groups, young at 3 months and aged at 12 months old; these mice received no treatment. Brains were aldehyde-fixed and processed for immunohistochemistry with various glial and neuronal markers. We found a clear reduction in glial cell number, both astrocytes and microglia, in the striatum after PBM in aged mice. By contrast, the number of 2 types of striatal interneurons (parvalbumin+ and encephalopsin+), together with the density of striatal dopaminergic terminals (and their midbrain cell bodies), remained unchanged after such treatment. In summary, our results indicated that long-term PBM had beneficial effects on the aging striatum by reducing glial cell number; and furthermore, that this treatment did not have any deleterious effects on the neurons and terminations in this nucleus

Crustal structure of the southern Dead Sea basin derived from project DESIRE wide-angle seismic data

As part of the DEad Sea Integrated REsearch project (DESIRE) a 235 km long seismic wide-angle reflection/refraction (WRR) profile was completed in spring 2006 across the Dead Sea Transform (DST) in the region of the southern Dead Sea basin (DSB). The DST with a total of about 107 km multi-stage left-lateral shear since about 18 Ma ago, accommodates the movement between the Arabian and African plates. It connects the spreading centre in the Red Sea with the Taurus collision zone in Turkey over a length of about 1100 km. With a sedimentary infill of about 10 km in places, the southern DSB is the largest pull-apart basin along the DST and one of the largest pull-apart basins on Earth. The WRR measurements comprised 11 shots recorded by 200 three-component and 400 one-component instruments spaced 300 m to 1.2 km apart along the whole length of the E-W trending profile. Models of the P-wave velocity structure derived from the WRR data show that the sedimentary infill associated with the formation of the southern DSB is about 8.5 km thick beneath the profile. With around an additional 2 km of older sediments, the depth to the seismic basement beneath the southern DSB is about 11 km below sea level beneath the profile. Seismic refraction data from an earlier experiment suggest that the seismic basement continues to deepen to a maximum depth of about 14 km, about 10 km south of the DESIRE profile. In contrast, the interfaces below about 20 km depth, including the top of the lower crust and the Moho, probably show less than 3 km variation in depth beneath the profile as it crosses the southern DSB. Thus the Dead Sea pull-apart basin may be essentially an upper crustal feature with upper crustal extension associated with the left-lateral motion along the DST. The boundary between the upper and lower crust at about 20 km depth might act as a decoupling zone. Below this boundary the two plates move past each other in what is essentially a shearing motion. Thermo-mechanical modelling of the DSB supports such a scenario. As the DESIRE seismic profile crosses the DST about 100 km north of where the DESERT seismic profile crosses the DST, it has been possible to construct a crustal cross-section of the region before the 107 km left-lateral shear on the DST occurred.</p

Neuroprotective effects of the gliopeptide ODN in an in vivo model of Parkinson’s disease

International audienceParkinson's disease (PD) is a neurodegenerative disorder characterized by a progressive loss of dopamine (DA) neurons through apoptotic, inflammatory and oxidative stress mechanisms. The octadecaneuropeptide (ODN) is a diazepam-binding inhibitor (DBI)-derived peptide, expressed by astrocytes, which protects neurons against oxidative cell damages and apoptosis in an in vitro model of PD. The present study reveals that a single intracerebroventricular injection of 10 ng ODN 1 h after the last administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) prevented the degeneration of DA neurons induced by the toxin in the substantia nigra pars compacta of mice, 7 days after treatment. ODN-mediated neuroprotection was associated with a reduction of the number of glial fibrillary acidic protein-positive reactive astrocytes and a strong inhibition of the expression of pro-inflammatory genes such as interleukins 1β and 6, and tumor necrosis factor-α. Moreover, ODN blocked the inhibition of the anti-apoptotic gene Bcl-2, and the stimulation of the pro-apoptotic genes Bax and caspase-3, induced by MPTP in the substantia nigra pars compacta. ODN also decreased or even in some cases abolished MPTP-induced oxidative damages, overproduction of reactive oxygen species and accumulation of lipid oxidation products in DA neurons. Furthermore, DBI knockout mice appeared to be more vulnerable than wild-type animals to MPTP neurotoxicity. Taken together, these results show that the gliopeptide ODN exerts a potent neuroprotective effect against MPTP-induced degeneration of nigrostriatal DA neurons in mice, through mechanisms involving downregulation of neuroinflammatory, oxidative and apoptotic processes. ODN may, thus, reduce neuronal damages in PD and other cerebral injuries involving oxidative neurodegeneration