Article ID Journal Published Year Pages File Type
2199227 Molecular and Cellular Neuroscience 2008 16 Pages PDF
Abstract

Electrical synapses, particularly gap junctions composed of connexin (Cx) 36, have been suggested to synchronize neuronal network oscillations. Recently, we generated Cx30.2-deficient mice which express β-galactosidase under control of Cx30.2 gene regulatory elements. In the central nervous system β-galactosidase activity representing Cx30.2 expression was restricted to NeuN-positive cells, thus identifying Cx30.2 as new neuronal connexin. In the hippocampus, co-immunofluorescence analyses revealed β-galactosidase/Cx30.2 expression in GABAergic inhibitory interneurons such as parvalbumin- and somatostatin-positive basket, axo-axonic, bistratified or oriens lacunosum-moleculare cells. ∼ 94% of the Cx30.2 expressing parvalbumin-positive interneurons also expressed Cx36. Performing field potential recordings from hippocampal slices we found no differences in basal excitation and excitation–inhibition balance between Cx30.2+/+ and Cx30.2LacZ/LacZ mice. Furthermore, frequency and power of gap junction dependent γ and ripples oscillations were similar in these animals. This suggests that the lack of Cx30.2 in interneurons can be largely compensated by other connexins, most likely Cx36.

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