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A deficiency of the link protein Bral2 affects the size of the extracellular space in the thalamus of aged mice
M. Cicanic, M. Edamatsu, Y. Bekku, I. Vorisek, T. Oohashi, L. Vargova,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články
PubMed
28815777
DOI
10.1002/jnr.24136
Knihovny.cz E-zdroje
- MeSH
- agrekany metabolismus MeSH
- analýza rozptylu MeSH
- difuzní magnetická rezonance MeSH
- extracelulární matrix - proteiny nedostatek genetika MeSH
- extracelulární prostor diagnostické zobrazování genetika MeSH
- gangliová stimulancia farmakologie MeSH
- kvartérní amoniové sloučeniny farmakologie MeSH
- messenger RNA MeSH
- myši inbrední C57BL MeSH
- myši transgenní MeSH
- myši MeSH
- neurony cytologie účinky léků MeSH
- novorozená zvířata MeSH
- proteiny nervové tkáně nedostatek genetika MeSH
- stárnutí fyziologie MeSH
- techniky in vitro MeSH
- thalamus cytologie MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
Bral2 is a link protein stabilizing the binding between lecticans and hyaluronan in perineuronal nets and axonal coats (ACs) in specific brain regions. Using the real-time iontophoretic method and diffusion-weighted magnetic resonance, we determined the extracellular space (ECS) volume fraction (α), tortuosity (λ), and apparent diffusion coefficient of water (ADCW ) in the thalamic ventral posteromedial nucleus (VPM) and sensorimotor cortex of young adult (3-6 months) and aged (14-20 months) Bral2-deficient (Bral2-/- ) mice and age-matched wild-type (wt) controls. The results were correlated with an analysis of extracellular matrix composition. In the cortex, no changes between wt and Bral2-/- were detected, either in the young or aged mice. In the VPM of aged but not in young Bral2-/- mice, we observed a significant decrease in α and ADCW in comparison with age-matched controls. Bral2 deficiency led to a reduction of both aggrecan- and brevican-associated perineuronal nets and a complete disruption of brevican-based ACs in young as well as aged VPM. Our data suggest that aging is a critical point that reveals the effect of Bral2 deficiency on VPM diffusion. This effect is probably mediated through the enhanced age-related damage of neurons lacking protective ACs, or the exhausting of compensatory mechanisms maintaining unchanged diffusion parameters in young Bral2-/- animals. A decreased ECS volume in aged Bral2-/- mice may influence the diffusion of neuroactive substances, and thus extrasynaptic and also indirectly synaptic transmission in this important nucleus of the somatosensory pathway.
Department of Neuroscience Charles University 2nd Faculty of Medicine Prague Czech Republic
Department of Neuroscience Institute of Experimental Medicine AS CR v v i Prague Czech Republic
Citace poskytuje Crossref.org
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- $a Bral2 is a link protein stabilizing the binding between lecticans and hyaluronan in perineuronal nets and axonal coats (ACs) in specific brain regions. Using the real-time iontophoretic method and diffusion-weighted magnetic resonance, we determined the extracellular space (ECS) volume fraction (α), tortuosity (λ), and apparent diffusion coefficient of water (ADCW ) in the thalamic ventral posteromedial nucleus (VPM) and sensorimotor cortex of young adult (3-6 months) and aged (14-20 months) Bral2-deficient (Bral2-/- ) mice and age-matched wild-type (wt) controls. The results were correlated with an analysis of extracellular matrix composition. In the cortex, no changes between wt and Bral2-/- were detected, either in the young or aged mice. In the VPM of aged but not in young Bral2-/- mice, we observed a significant decrease in α and ADCW in comparison with age-matched controls. Bral2 deficiency led to a reduction of both aggrecan- and brevican-associated perineuronal nets and a complete disruption of brevican-based ACs in young as well as aged VPM. Our data suggest that aging is a critical point that reveals the effect of Bral2 deficiency on VPM diffusion. This effect is probably mediated through the enhanced age-related damage of neurons lacking protective ACs, or the exhausting of compensatory mechanisms maintaining unchanged diffusion parameters in young Bral2-/- animals. A decreased ECS volume in aged Bral2-/- mice may influence the diffusion of neuroactive substances, and thus extrasynaptic and also indirectly synaptic transmission in this important nucleus of the somatosensory pathway.
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