In rodents, whisker deprivation induces changes in neuronal responses in the somatosensory barrel cortex called Experience dependent plasticity (EDP). There are two general forms of synaptic EDP: Hebbian, and Homeostatic. Our aim was to determine the role of astrocytes in these processes, using in vivo whisker deprivation and ex vivo fEPSP recordings. In response to a week of unilateral all-whisker sensory deprivation of one side of the snout, a PKA-dependent form of long term potentiation (LTP) emerges at L4-L2/3 synapses in the contralateral barrel cortex, in addition to the NMDA receptor dependent LTP observed in undeprived animals. PKA-dependent LTP was also present in undeprived barrel cortex of an astrocyte IP3R2 genetic deletion mouse, indicating an astrocytic involvement in this process. To test the role of astrocyte cytoplasmic calcium signaling in vivo, the plasma membrane calcium extrusion pump CalEx was selectively overexpressed by AAV transfection in barrel cortex astrocytes of wild type mice. This mimicked the effect of whisker deprivation in inducing the emergence of a PKA dependent LTP mechanism but in whisker intact animals, indicating that reducing cytosolic calcium is sufficient to invoke this homeostatic response. Since BDNF has been implicated in EDP mediated changes we conducted experiments where during whisker deprivation, the agonist DHF was injected. This prevented the emergence of the PKA dependent LTP, also indicating a role for TRkB receptor signalling.These findings place astrocytes as sensors and mediators of whisker sensory experience- dependent plasticity in the brain.