Clinical evidence suggests that cortical excitability is increased in depressives. We investigated its cellular basis in a mouse model of depression. In a modified version of forced swimming (FS), mice were initially forced to swim for 5 consecutive days and then were treated daily with repetitive transcranial magnetic stimulation (rTMS) or sham treatment for the following 4 weeks without swimming. On day 2 through day 5, the mice manifested depression-like behaviors. The next and last FS was performed 4 weeks later, which revealed a 4 week maintenance of depression-like behavior in the sham mice. In slices from the sham controls, excitability in cingulate cortex pyramidal cells was elevated in terms of membrane potential and frequencies of spikes evoked by current injection. Depolarized resting potential was shown to depend on suppression of large conductance calcium-activated potassium (BK) channels. This BK channel suppression was confirmed by measuring spike width, which depends on BK channels. Chronic rTMS treatment during the 4 week period significantly reduced the depression-like behavior. In slices obtained from the rTMS mice, normal excitability and BK channel activity were recovered. Expression of a scaffold protein Homer1a was reduced by the FS and reversed by rTMS in the cingulate cortex. Similar recovery in the same behavioral, electrophysiological, and biochemical features was observed after chronic imipramine treatment. The present study demonstrated that manifestation and disappearance of depression-like behavior are in parallel with increase and decrease in cortical neuronal excitability in mice and suggested that regulation of BK channels by Homer1a is involved in this parallelism.

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The region of vibrissae representation in the ventrobasal complex (VB) of the rat was systematically mapped, based on receptive fields of many single neurons. Results showed that the ventralmost row of vibrissae projected to the rostral part of VB, that the dorsal-most row projected to the caudal part, and that the caudalmost vibrissae of each row projected to the most dorsolateral part of VB and more rostral vibrissae to the more ventromedial part. Further, it was revealed that the clusters of neurons receiving projections from any individual vibrissae formed corresponding columns extending from the anterodorsomedial to the posteroventrolateral direction, and that these columns piled up dorsoventrally and anteroposteriorly, with ventral ones shifted progressively medially. When cross sections of these columns were viewed on an oblique horizontal section of VB, a group of columns corresponding to each row lined up from the dorsolateral to the ventromedial direction with a rostral convexity, which means that the third or fourth vibrissa in each row projected most rostrally in that row. These results confirmed previous physiological mapping studies of vibrissal representation and are in good agreement with anatomical studies on barreloid structure in VB.

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