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Cerebral Cortex, Vol. 10, No. 7, 684-697, July 2000
© 2000 Oxford University Press

Myelination Defects and Neuronal Hyperexcitability in the Neocortex of Connexin 32-deficient Mice

Bernd Sutor, Cordula Schmolke1,2, Barbara Teubner3, Clemens Schirmer and Klaus Willecke3

Institute of Physiology, University of Munich, Pettenkoferstrasse 12, D-80336 Munich, , 1 Institute of Anatomy, University of Bonn, Nussallee 10, D-53115 Bonn and , 3 Institute of Genetics, University of Bonn, Römerstrasse 164, D-53117 Bonn, Germany

Morphological and electrophysiological studies were performed on neocortices of adult Connexin 32 (Cx32)-deficient mice and wild-type mice to investigate the consequences of a lack of the gap junction subunit Cx32 on neocortical structure and function. Morphometrical analysis revealed a reduced volume fraction of myelin within the neuropil and a decreased thickness of the axonal myelin sheaths in the neocortex of Cx32-deficient mice. Intracellular recordings from neurons in neocortical slice preparations provided evidence for an increased membrane input resistance in neurons of Cx32-null mutant mice as compared to neurons of wild-type mice. Consequently, neurons of Cx32-deficient mice displayed an enhanced intrinsic excitability. In addition, ~50% of the neurons investigated in slices of Cx32-deficient mice responded to afferent stimulation with delayed and large glutamatergic excitatory postsynaptic potentials resembling paroxysmal depolarizations. GABAergic inhibition sufficient to efficiently control synaptic excitability was virtually absent in these cells. The changes in intrinsic membrane properties observed in neurons of Cx32-null mutant mice were independent of the alterations in synaptic function, since increased membrane resistances were observed also in neurons with normal synaptic response pattern. Thus, in the neocortex, lack of Cx32 correlates with myelination defects, alterations in intrinsic membrane properties and dysfunction of inhibitory synaptic transmission.


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