A deficiency of the link protein Bral2 affects the size of the extracellular space in the thalamus of aged mice
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
28815777
DOI
10.1002/jnr.24136
Knihovny.cz E-resources
- Keywords
- Bral2, aging, diffusion, extracellular matrix, extracellular space,
- MeSH
- Aggrecans metabolism MeSH
- Analysis of Variance MeSH
- Diffusion Magnetic Resonance Imaging MeSH
- Extracellular Matrix Proteins deficiency genetics MeSH
- Extracellular Space diagnostic imaging genetics MeSH
- Ganglionic Stimulants pharmacology MeSH
- Quaternary Ammonium Compounds pharmacology MeSH
- RNA, Messenger MeSH
- Mice, Inbred C57BL MeSH
- Mice, Transgenic MeSH
- Mice MeSH
- Neurons cytology drug effects MeSH
- Animals, Newborn MeSH
- Nerve Tissue Proteins deficiency genetics MeSH
- Aging physiology MeSH
- In Vitro Techniques MeSH
- Thalamus cytology MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Mice MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Aggrecans MeSH
- Extracellular Matrix Proteins MeSH
- Ganglionic Stimulants MeSH
- Hapln4 protein, mouse MeSH Browser
- Quaternary Ammonium Compounds MeSH
- RNA, Messenger MeSH
- Nerve Tissue Proteins MeSH
- tetramethylammonium MeSH Browser
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
NYU Neuroscience Institute New York University Langone Medical Center New York USA
References provided by Crossref.org
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