Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2199227 | Molecular and Cellular Neuroscience | 2008 | 16 Pages |
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.