Synaptic alpha-dystrobrevin: Localization of a short alpha-dystrobrevin isoform in melanin-concentrating hormone neurons of the hypothalamus

Abstract The expression of the two members of the dystrobrevin (DB) family in the adult brain was thought to be highly specific for the two main cell types: alpha-dystrobrevin (α-DB) and beta-dystrobrevin (β-DB) has been identified as glial and neuronal proteins, respectively. In the present work we...

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Veröffentlicht in:Brain research 2008-03, Vol.1201, p.52-59
Hauptverfasser: Hazai, Diana, Lien, Chun-Fu, Hajós, Ferenc, Halasy, Katalin, Górecki, Dariusz C, Jancsik, Veronika
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Sprache:eng
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Zusammenfassung:Abstract The expression of the two members of the dystrobrevin (DB) family in the adult brain was thought to be highly specific for the two main cell types: alpha-dystrobrevin (α-DB) and beta-dystrobrevin (β-DB) has been identified as glial and neuronal proteins, respectively. In the present work we show that a subset of neurons in the hypothalamus contains α-DB. Comparative immunohistochemical studies with two α-DB antibodies of different specificity indicate that the neurons contain short α-DB isoform(s) α-DB-2 and/or α-DB-4. Immunoreactive multipolar or spindle-shaped neurons form clusters with bilateral symmetry, localized predominantly in the lateral hypothalamic area, with extensions into the zona incerta and the dorso-medial and ventro-medial hypothalamic region. α-DB immunoreactivity was localized in cell processes and at postsynaptic densities, furthermore in the endoplasmic reticulum within the perikarya. α-DB-positive neurons are β-dystrobrevin immunoreactive, but α- and β-DB do not co-localize with their usual molecular anchors like dystrophins or high molecular weight forms of utrophin. Colocalization with nNOS was also not observed. The pattern of α-DB immunoreactive neurons gave a perfect colocalization with melanin-concentrating hormone (MCH) neurons throughout the whole region studied. We propose that α-DB plays a role in a structure or regulation mechanism unique to MCH-expressing neurons.
ISSN:0006-8993
1872-6240
DOI:10.1016/j.brainres.2008.01.046