Astrocytic calcium (Ca2+) signaling is required for the long-lasting facilitatory action of endocannabinoids (eCB) upon transmitter release from pyramidal hippocampal neurons, a form of long-term potentiation (LTP) known as eCB-LTP, which does not involve NMDA receptors (NMDAR). Astrocytic type one cannabinoid receptors (CB1R) are also required for “classical” forms of LTP but whether astrocytic Ca2+ signaling is a requisite this action of CB1R is poorly known. Adenosine A1 receptor (A1R) modulates CB1R activity in neurons, but the consequences of the astrocytic Ca2+ signaling for the A1R-CB1R crosstalk and its impact in LTP are also unknown. Thus, we aimed at evaluating whether CB1R-mediated astrocytic Ca2+ signaling impacts theta-burst-induced LTP at hippocampal CA3-CA1 synapses and how it is affected by A1R. We used IP3R2-KO mice, which lack IP3R2-mediated astrocytic Ca2+ signaling, in comparison with wild-type littermates (IP3R2-WT). We show that while the absence of IP3R2-mediated astrocytic Ca2+ signaling does not impact LTP, it does reduce the protein levels of NMDAR-NR2B subunit. Exogenous activation or blockade of CB1R reduced LTP in IP3R2-WT mice, while in IP3R2-KO mice LTP levels were not significantly affected by CB1R activation. Blocking A1R reduced LTP in both IP3R2-WT and IP3R2-KO mice, and prevented the inhibition caused by exogenous CB1R activation in IP3R2-WT mice but not in IP3R2-KO mice. Our data demonstrates that the inhibition of hippocampal LTP by exogenous CB1R activation requires astrocytic calcium signaling, which also play a role in the CB1R/A1R interaction. This work thus adds novel partners to synaptic plasticity modulation by cannabinoids.