Figure 8.

EC lesion-induced dentate hyperactivity is normalized by optogenetic stimulation of the cholinergic sprouting. A, Lesioned mice at 7 and 30 dpl and sham-operated mice showed spontaneous dentate LFP spikes that were visible in raw LFP traces, especially in DG layers (top). These spontaneous events were associated with a strong CSD sink located in the dentate molecular layer. Both CSD and LFP signals associated with spontaneous dentate LFP spikes strongly resembled pp-evoked responses, suggesting that EC inputs contributed to dentate LFP spikes. Arrows indicate dentate LFP spikes or pp stimulations. B, Under baseline conditions, lesioned mice at both 7 and 30 dpl had an increased frequency of dentate LFP spikes that was normalized by local optical stimulation of cholinergic terminals within the dHPC. C, Lesioned mice from both postlesion delays had increased CSD pp-like sink frequency (3SD above mean sink amplitude) in the deafferented DG molecular layer that was also normalized by local optical stimulation. D, Multiunit spontaneous firing frequency was three times higher in lesioned mice than in sham mice at 30 dpl. However, the firing frequency was also normalized to sham level by local optical stimulation. $p < 0.05, $$p < 0.01, $$$p < 0.001, **p < 0.01, ***p < 0.001, each differs from baseline (Newman–Keuls); n indicates the number of animals in each group, except for D, where it refers to the number of cells recorded.