Coupling characteristics in KO and dKO mice for the major oligodendrocytic and astrocytic gap junctions that participate in glial networks. A. There are some discrepancies about the major connexin subtype mediating O/O coupling. Maglione et al. [64] found a pronounced reduction in O/O coupling in Cx47 deficient mice but it was unaffected in Cx32 deficient mice while Wasseff and Scherer [67] results suggest the opposite. The later authors discuss that discrepancies can be due to methodological aspects as the dye used in the permeability assays was different in both studies as well as the genetic background of the mice used as control. However, both investigations agree in the finding that no O/O coupling remains in either the corpus callosum or neocortex of Cx47/Cx32 dKO mice. Maglione et al. [64] further inspected O/O coupling in Cx30/Cx43 dKO which was found to be reduced. The lack of Cx43 alone diminished the coupling of oligodendrocytes to immature oligodendrocyte subpopulation suggesting a role for astrocytic Cx43 in precursor population progression. B. Studies from Maglione et al. [64] and Wasseff and Scherer [67] failed to find robust O/A coupling in the corpus callosum in contraposition to the traditional view that oligodendrocytes were only coupled to astrocytes. However, the weak O/A coupling observed in control mice was reduced in Cx47 deficient mice and totally abolished in Cx47/Cx32 dKO and Cx30/Cx43 dKO. C. Conditional deletion of Cx43 in astrocytes results in 50% decay [74] of the A/A coupling in the hippocampus while loss of Cx30 causes 20% reduction [71] on the astroglial hippocampal coupling. However, A/A coupling is completely impaired by the deletion of both astrocytic connexins [72].