How functional columns are synchronized or desynchronized is an essential question on columnar integration. It has been reported that 5-Hz synchronous network oscillation was activated by acute application of kainic acid in layer (L) 2/3 in the barrel cortex. We have recently reported that GABA_B-mediated presynaptic inhibition of intracortical inputs (GABA_B-Pre-I) was involved in inter-columnar desynchronization in the barrel cortex using dual whole-cell recordings from two L3 PCs in the adjacent columns (Sato et al., 2013). In the present study, by using voltage-sensitive dye (RH414) imaging methods in slice preparations of the rat barrel cortex, we addressed how GABA_B-Pre-I of intracortical inputs modulates the spatio-temporal pattern of oscillatory synchronization of the activity of L2/3 pyramidal cells. When a paired microstimulation at 200-ms interval was applied to L2/3 of a column in the presence of bicuculline and APV, the horizontal spread of the excitation in L2/3 extended beyond the distal end of the neighboring columns after the 1st stimulation, resulting in the excitation in L5 of the same columns that exhibited synchronous excitation in L2/3. The horizontal excitation spread in L3 appeared to be depressed in the 2nd response compared to the 1st response. CGP55845 converted such a spatial PPD into a PPF, which resulted in a marked enhancement of the 2nd response in L5. This enhancement of excitation spread by CGP may be caused largely by a release from inter-columnar desynchronization because more synchronous activation of L2/3 PCs induces more activation of L5 PCs. Thus, GABA_B-Pre-I is likely to be involved in the desynchronization of spike activities between the two neuronal populations in mutually adjacent columns. Bath application of kainic acid induced an oscillatory synchronous excitation across the multiple columns. Both kainate receptor antagonist and CGP55845 abolished the oscillatory synchronization. It is possible that the oscillatory synchronization in L2/3 is mediated by the interaction between the activation of kainite receptors and GABA_B-Pre-I.