Literature DB >> 10197766

Connexin30 in rodent, cat and human brain: selective expression in gray matter astrocytes, co-localization with connexin43 at gap junctions and late developmental appearance.

J I Nagy1, D Patel, P A Ochalski, G L Stelmack.   

Abstract

We previously presented evidence [Nagy et al. (1997) Neuroscience 78, 533-548] that, in addition to their ubiquitous expression of connexin43, astrocytes produce a second connexin suggested to be connexin30, a recently discovered member of the family of gap junction proteins. A connexin30 specific antibody was subsequently developed and utilized here to confirm and extend our earlier observations. On western blots, this antibody detected a 30,000 mol. wt protein in rat, mouse, cat and human brain, and exhibited no cross-reaction with connexin43, connexin26 or any other known connexins expressed in brain. Immunohistochemically, connexin30 was localized in astrocytes, at gap junctions between these cells and on the astrocyte side of gap junctions between astrocytes and oligodendrocytes. Double labelling revealed co-localization of connexin30 and connexin43 at astrocytic gap junctions. Punctate immunolabelling patterns for both connexins were qualitatively similar, but differences were evident. In contrast to regional connexin43 expression, diencephalic and hindbrain areas exhibited considerably greater expression than forebrain areas, subcortical perivascular astrocytic endfeet were more heavily labelled for connexin30, white matter tracts such as corpus callosum, internal capsule and anterior commissure were devoid of connexin30, and appreciable levels of connexin30 during development were not seen until about postnatal day 15. These results indicate that connexin30 is expressed by gray, but not white matter astrocytes, its distribution is highly heterogeneous in gray matter, it is co-localized with connexin43 at astrocytic gap junctions where it forms homotypic or heterotypic junctions, and its emergence is delayed until relatively late during brain maturation. Taken together, these results suggest that astrocytic connexin30 expression at both regional and cellular levels is subject to regulation in adult brain as well as during brain development.

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Year:  1999        PMID: 10197766     DOI: 10.1016/s0306-4522(98)00191-2

Source DB:  PubMed          Journal:  Neuroscience        ISSN: 0306-4522            Impact factor:   3.590


  114 in total

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2.  Astrocyte and oligodendrocyte connexins of the glial syncytium in relation to astrocyte anatomical domains and spatial buffering.

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4.  Connexin 30 expression inhibits growth of human malignant gliomas but protects them against radiation therapy.

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5.  EphA4 deficient mice maintain astroglial-fibrotic scar formation after spinal cord injury.

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Review 6.  Life cycle of connexins in health and disease.

Authors:  Dale W Laird
Journal:  Biochem J       Date:  2006-03-15       Impact factor: 3.857

7.  Characterisation of Peptide5 systemic administration for treating traumatic spinal cord injured rats.

Authors:  Yilin Mao; Tara Nguyen; Ryan S Tonkin; Justin G Lees; Caitlyn Warren; Simon J O'Carroll; Louise F B Nicholson; Colin R Green; Gila Moalem-Taylor; Catherine A Gorrie
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8.  Connexin 30 sets synaptic strength by controlling astroglial synapse invasion.

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Review 9.  Role of connexin-based gap junction channels and hemichannels in ischemia-induced cell death in nervous tissue.

Authors:  Jorge E Contreras; Helmuth A Sánchez; Loreto P Véliz; Feliksas F Bukauskas; Michael V L Bennett; Juan C Sáez
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Review 10.  Modulation of brain hemichannels and gap junction channels by pro-inflammatory agents and their possible role in neurodegeneration.

Authors:  Juan A Orellana; Pablo J Sáez; Kenji F Shoji; Kurt A Schalper; Nicolás Palacios-Prado; Victoria Velarde; Christian Giaume; Michael V L Bennett; Juan C Sáez
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