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Synaptic plasticity is postulated to be the basis of learning and memory. Although pre- and post-synaptic mechanisms of various forms of synaptic plasticity have been investigated in detail, the contribution of astrocytes has remained controversial. Electrical stimulation of the nucleus basalis of Meynert (NBM) transiently changes the synchronized EEG state (UP/DOWN states) to the desynchronized state in the cerebral cortex and such changes are abolished by the muscarinic acetylcholine receptor antagonist atropine. In urethane anesthetized C57BL6 mouse barrel cortex, local field potential response to whisker deflection became significantly larger when the sensory stimulation was combined with electrical stimulation of the NBM. The enhancement of synaptic response was blocked by topical application of atropine, suggesting that activation of the cholinergic projection plays a significant role.

Layer 2/3 cortical astrocytes showed increases of intracellular Ca2+ concentration in response to NBM stimulation, as observed with in vivo two-photon microscopy. Such Ca2+ increases were diminished by atropine or in inositol 1,4,5-trisphosphate receptor type 2 (IP3R2) knockout mice. Although IP3R2 knockout mice showed similar transient desynchronized EEG by NBM stimulation, conjunctive presentation of sensory stimulation and NBM stimulation did not produce an enhanced local field potential response in IP3R2 knockout mice. Our results provide in vivo evidence for possible involvement of astrocytic Ca2+ activity in the sensory and acetylcholine dependent synaptic plasticity.