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The Journal of Neuroscience, October 1, 2001, 21(19):7534-7542
Global Ischemia-Induced Increases in the Gap Junctional Proteins
Connexin 32 (Cx32) and Cx36 in Hippocampus and Enhanced Vulnerability
of Cx32 Knock-Out Mice
Keiji
Oguro,
Teresa
Jover,
Hidenobu
Tanaka,
Ying
Lin,
Takashi
Kojima,
Noriko
Oguro,
Sonja Y.
Grooms,
Michael V. L.
Bennett, and
R. Suzanne
Zukin
Department of Neuroscience, Albert Einstein College of Medicine,
Bronx, New York 10461
Gap junctions are conductive channels that connect the interiors of
coupled cells. In the hippocampus, GABA-containing hippocampal interneurons are interconnected by gap junctions, which mediate electrical coupling and synchronous firing and thereby promote inhibitory transmission. The present study was undertaken to examine the hypothesis that the gap junctional proteins connexin 32 (Cx32; expressed by oligodendrocytes, interneurons, or both), Cx36 (expressed by interneurons), and Cx43 (expressed by astrocytes) play a role in
defining cell-specific patterns of neuronal death in hippocampus after
global ischemia in mice. Global ischemia did not significantly alter
Cx32 and Cx36 mRNA expression and slightly increased Cx43 mRNA
expression in the vulnerable CA1, as assessed by Northern blot analysis
and in situ hybridization. Global ischemia induced a
selective increase in Cx32 and Cx36 but not Cx43 protein abundance in
CA1 before onset of neuronal death, as assessed by Western blot
analysis. The increase in Cx32 and Cx36 expression was intense and
specific to parvalbumin-positive inhibitory interneurons of CA1, as
assessed by double immunofluorescence. Protein abundance was unchanged
in CA3 and dentate gyrus. The finding of increase in connexin protein
without increase in mRNA suggests regulation of Cx32 and Cx36
expression at the translational or post-translational level. Cx32(Y/ )
null mice exhibited enhanced vulnerability to brief ischemic insults,
consistent with a role for Cx32 gap junctions in neuronal survival.
These findings suggest that Cx32 and Cx36 gap junctions may contribute
to the survival and resistance of GABAergic interneurons, thereby
defining cell-specific patterns of global ischemia-induced neuronal death.
Key words:
gap junctions; neural connexins; global ischemia; neuronal death; GABAergic interneurons; electrical transmission; Cx32
knock-out
Copyright © 2001 Society for Neuroscience 0270-6474/01/21197534-09$05.00/0
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