Our study suggests that BDNF from CA3 pyramidal neurons does not affect these oscillations in CA3, but facilitates them in CA1 by attenuating expression and activity of 5-HT3 receptor, which is expressed in a subpopulation of PV-negative GABAergic neurons, but not in the principal neurons. Several observations suggest that BDNF facilitates oscillatory activity. In cultured hippocampal neurons, it increases fidelity of spikes during periodic current injections and facilitates spontaneous Ca2+ oscillations ; in developing cortical neurons, it potentiates frequency of synchronous spontaneous oscillations. BDNF also modulates GABAergic transmission, which underlies oscillatory activities, but, to our knowledge, there has been no direct evidence so far that BDNF influences oscillations through GABAergic neurons. The Ergosterol present study provides such evidence and suggests that the effect is Dirithromycin mediated by serotonergic system. First, gamma oscillations were attenuated in slices from KO mice. Second, in these slices, 5-HT enhanced sIPSCs more strongly than in control slices, but this difference was attenuated by a HT3 receptor antagonist, which also reversed the oscillation deficit. These data suggest that the up-regulation of 5-HT3 receptor and subsequent changes in GABAergic neurons, which express this receptor, were responsible for attenuated oscillations in slices from KO mice. However, the reversal of oscillation deficit by 5-HT3 receptor antagonist was only partial, possibly because of irreversible changes caused by chronic up-regulation of 5-HT3 receptor. The partial rescue may also indicate that BDNF regulates gamma oscillations through additional 5-HT3 receptor-independent mechanisms, for example, by directly modulating fast-spiking interneurons. We could not reverse the oscillation deficit by acute application of recombinant BDNF. It is consistent with the idea that effect of BDNF on gamma oscillations is indirect and may be mediated by molecules like 5-HT3 receptor, whose expression or activity are altered during long-lasting reduction in BDNF concentration in KO mice and cannot be reversed rapidly. Surprisingly, in contrast to the oscillation deficit in CA1, slices from KO animals had normal oscillations in CA3, despite the deletion of BDNF gene in this area. This difference may result from the lower serotonergic innervations of the CA3 pyramidal layer, which may render CA3 oscillations less dependent on 5-HT than the oscillations in area CA1, which has more serotonergic axons. Such explanation is consistent with an idea that the main effect of BDNF on oscillations is mediated by serotonergic system. Changes in gamma oscillations have been found in several brain illnesses, including schizophrenia, bipolar disorder and Alzheimer, some of which include cognitive impairments.