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Neuronal oscillations and their inter‐areal synchronization may be instrumental in regulating neuronal communication in distributed networks. Several lines of research have, however, shown that cognitive tasks engage neuronal oscillations simultaneously in multiple frequency bands that have distinct functional roles in cognitive processing. Gamma oscillations (30–120 Hz) are associated with bottom‐up processing, while slower oscillations in delta (1–4 Hz), theta (4–7 Hz), alpha (8–14 Hz) and beta (14–30 Hz) frequency bands may have roles in executive or top‐down controlling functions, although also other distinctions have been made. Identification of the mechanisms that integrate such spectrally distributed processing and govern neuronal communication among these networks is crucial for understanding how cognitive functions are achieved in neuronal circuits. Cross‐frequency interactions among oscillations have been recognized as a likely candidate mechanism for such integration. We advance here the hypothesis that phase–phase synchronization of neuronal oscillations in two different frequency bands, cross‐frequency phase synchrony (CFS), could serve to integrate, coordinate and regulate neuronal processing distributed into neuronal assemblies concurrently in multiple frequency bands. A trail of studies over the past decade has revealed the presence of CFS among cortical oscillations and linked CFS with roles in cognitive integration. We propose that CFS could connect fast and slow oscillatory networks and thereby integrate distributed cognitive functions such as representation of sensory information with attentional and executive functions. Coupling of fast (red) and slow (blue) oscillations by cross‐frequency phase synchrony (CFS) may enable consistent spike timing between assemblies oscillating in different frequencies. Phase lags promoting coinciding neuronal spiking could incur a stronger post‐synaptic impact in downstream neurons than uncorrelated inputs. At the network level, CFS could support the functional integration of fast and slow neuronal oscillatory networks by connecting key hubs of the 1:1 synchronized networks. [ABSTRACT FROM AUTHOR]

Spontaneous transients of correlated activity are a characteristic feature of immature brain structures, where they are thought to be crucial for the establishment of precise neuronal connectivity. Studies on experimental animals have shown that this kind of early activity in cortical structures is composed of long-lasting, intermittent network events, which undergo a developmental decline that is closely paralleled by the maturation of GABAergic inhibition. In order to examine whether similar events occur in the immature human cortex, we performed direct current-coupled electroencephalography (EEG) recordings from sleeping preterm babies. We show now that much of the preterm EEG activity is confined to spontaneous, slow activity transients. These transients are characterized by a large voltage deflection that nests prominent oscillatory activity in several frequency bands covering the whole frequency spectrum of the preterm EEG (<0.1–30 Hz). The slow voltage deflections had an amplitude of up to 800 µV. Most of these ‘giant’ events originated in the temporo-occipital areas, with a maximum rate of about 8/min, and their occurrence as well as amplitude showed a decline by the time of normal birth. In age-matched fetal brain tissue, this decrease in the spontaneous activity transients was associated with a developmental up-regulation of the neuronal chloride extruder K+–Cl− cotransporter 2, a crucial molecule for the generation of inhibitory GABAergic Cl– currents. Our work indicates that slow endogenous activity transients in the immature human neocortex are mostly confined to the prenatal stage and appear to be terminated in parallel with the maturation of functional GABAergic inhibition. [ABSTRACT FROM AUTHOR]