It is known that astrocytes, by the Ca2+-dependent release of gliotransmitters, which then act in pre- and post-synaptic receptors, modulate neuronal transmission and plasticity. Thus, hippocampal θ-burst long-term potentiation (LTP), which is a form of synaptic plasticity, can be modulated by astrocytes, since these cells release gliotransmitters that are crucial for the maintenance of LTP. Therefore, in this study, we hypothesized that the facilitatory action of BDNF upon LTP would involve astrocytes. To address that possibility, fEPSP recordings were performed in CA3-CA1 area of hippocampal slices from three different experimental models: Wistar rats where astrocytic metabolism was selectively reduced by a gliotoxin, the DL-fluoricitric acid (FC), IP3R2-/- mice model, which lack IP3R2-mediated Ca2+-signaling in astrocytes and dn-SNARE transgenic mice, in which the SNARE-dependent release of gliotransmitters. For the three models we observed that the astrocytic impairment abolished the excitatory BDNF effect upon hippocampal LTP, only while inducing LTP with a mild θ-burst stimulation paradigm. The present data shows for the first time that astrocytes play an active role in the facilitatory action of BDNF upon LTP, depending on stimulation paradigm.
Different doses of methamphetamine alter long-term potentiation, level of BDNF and neuronal apoptosis in the hippocampus of reinstated rats