74% ± 4.75% of stimulations in the PL. The evoked SB started in the Cg 102 ± 10 ms and in the PL 103.1 ± 7.7 ms after the onset of stimulus (Figures 7B and 7C). Similar results were obtained when repetitive stimulation at 10 or 100 Hz was used. The effect of electrical stimulation on the CA1 region might be strengthened by costimulation of the neighboring alvear pathway (Deller et al., 1996). Remarkably, the occurrence of evoked SB increased on the anterior-posterior axis (Figure S7B), confirming that the density of functional projections to the PFC increases from the dorsal

to ventral Hipp (Hoover and Vertes, 2007). These data indicate that hippocampal projections that innervate the neonatal PFC selleck kinase inhibitor are an ideal candidate for mediating the hippocampal drive to the PFC. To confirm the contribution of hippocampal drive to the generation of oscillatory rhythms in the neonatal PFC, three experimental approaches were additionally used. In the first instance, the intermediate and ventral but not dorsal Hipp were excitotoxically lesioned at P1, and the consequences on prefrontal-hippocampal networks were investigated at the end of the first postnatal week. Neonatal rats (n = 12) received a small volume (20–50 nl) of 40 mM buy Erastin NMDA (lesioned pups) or of 0.1 M PBS (sham pups) according to a previously

described protocol (Lipska et al., 1993). The features of the NMDA-induced lesion were assessed post-mortem after Nissl staining. Characteristic cavitation, tissue loss, and gliosis (Bertrand et al., 2010) were present in lesioned pups, but not in the PBS-treated pups. The lesion extent, however, differed considerably across animals (Figures 8A and 8B). The CA1 and CA3 areas of the intermediate and ventral, but not dorsal Hipp were mainly affected. In some cases (n = 2), damage extended to the neighboring EC (Figure 8A). Moreover, lesions were mostly associated with a robust enlargement of the lateral ventricles. Because

an excitotoxic lesion may generally impair the development of pups by affecting their behavior and feeding abilities, we investigated the developmental milestones of PBS- and NMDA-treated animals. Their daily weight gain and general behavior (sleep-awake either cycle, righting and grasping reflexes, feeding and locomotor behavior) were similar, indicating that the excitotoxic lesion did not impair the neonatal development. Whereas PBS treatment of the Hipp did not modify the features of prefrontal SB and NG, NMDA-induced lesion affected them. The occurrence of cingulate and prelimbic SB as well as of cingulate NG slightly decreased after hippocampal lesion, yet not at significant level. More prominent were the NMDA effects on the occurrence of prelimbic NG that decreased from 0.65 ± 0.16 bursts/min in PBS-treated pups to 0.06 ± 0.04 bursts/min (p < 0.05) (Figure 8C). The amplitude, duration, and main frequency of SB and NG did not change after NMDA lesion.