6 ± 0.9 to 3.6 ± 0.8 (n = 8 pups, p < 0.05). Consequently, the occurrence of prelimbic NG decreased from 1.1 ± 0.2 bursts/min in ACSF-treated pups to 0.6 ± 0.24 bursts/min (p < 0.05), while cingulate activity and prelimbic SB remained unaffected (Figure 8H). The results of the three experimental approaches indicate that impairment of the Hipp, independently of the induction method, strongly reduces the early network activity of the PL. Oscillatory entrainment of adult prefrontal-hippocampal networks seems to efficiently ensure reciprocal information transfer associated with mnemonic and executive functions. In the present study, we used multielectrode recordings to elucidate when and how

this oscillatory entrainment between the PFC and Hipp develops through life and to get first insights into its mechanisms MEK inhibitor cancer and function. We demonstrate here for

the first time that the rat PFC starts to generate bursts of oscillatory activity with subregion-specific spatial and temporal organization during the first postnatal week. We additionally provide experimental evidence that this discontinuous prefrontal activity Selleckchem GSK2656157 is driven via synaptic projections by hippocampal theta bursts. With ongoing maturation of the PFC and switch from discontinuous bursts to continuous theta-gamma rhythms, reciprocal interactions start to synchronize the prejuvenile prefrontal and hippocampal networks in theta oscillatory rhythms. These data indicate that the prefrontal and hippocampal networks maturate tightly correlated by transient coupling in oscillatory rhythms. During the first two postnatal weeks, the network activity of the rodent PFC undergoes prominent changes, the initially generated discontinuous oscillations being replaced by continuous rhythms. This developmental time window corresponds Histamine H2 receptor to a period of massive cytoarchitectonic and functional reorganization of the PFC and its connectivity. Extending over approximately 3 weeks in rodents and until adolescence in humans (Flechsig, 1901 and Van Eden and Uylings, 1985), the maturation of the PFC is significantly

prolonged when compared with that of the primary sensory cortices. Correspondingly, the emergence of oscillatory bursts in the PFC, first observed at P3, is delayed when compared with the onset around birth of activity patterns in the V1 or S1 (Hanganu et al., 2006 and Yang et al., 2009). These oscillations recorded in urethane-anesthetized rats mirror the physiological activity patterns of the developing PFC, since urethane anesthesia mimics the full spectrum of the natural sleep (Clement et al., 2008) and neonatal rats spend most of their time sleeping (Bolles and Woods, 1964). Therefore, it is not surprising that the incidence and most of the properties of neonatal SB were independent of the presence or level of urethane-anesthesia (see also Yang et al., 2009).