Temporally-structured cortical activity in the form of synchronized network oscillations and persistent activity is fundamental for cognitive processes such as sensory processing, motor control, working memory, and consolidation of long-term memory. The roles of fast glutamatergic excitation via AMPA, kainate, and NMDA receptors, as well as fast GABAergic inhibition via GABA(A) receptors, in such network activity have been studied in great detail. In contrast, we have only recently begun to appreciate the roles of slow inhibition via GABA(B) receptors in the control of cortical network activity. Here, we provide a framework for understanding the contributions of GABA(B) receptors in helping mediate, modulate, and moderate different types of physiological and pathological cortical network activity. We demonstrate how the slow time course of GABA(B) receptor-mediated inhibition is well suited to help mediate the slow oscillation, to modulate the power and spatial profile of gamma oscillations, and to moderate the relative spike timing of individual neurons during theta oscillations. We further suggest that GABA(B) receptors are interesting therapeutic targets in pathological conditions where cortical network activity is disturbed, such as epilepsy and schizophrenia.
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