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. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: Cell Calcium. 2013 Sep 24;54(6):10.1016/j.ceca.2013.09.001. doi: 10.1016/j.ceca.2013.09.001

Fig. 5.

Fig. 5

Diagram illustrating two possible mechanisms driving astrocytic Ca2+ responses in awake, head-restrained mice. (A) The tripartite synapse model: Here, astrocytes respond to local neuronal activity and neurotransmitter release with spotty, asynchronous increases in [Ca2+]i. (B) The neuromodulator model: Following novel or noxious behavioral stimuli, neuromodulators are released throughout the cortex to rapidly alter network connectivity. Our data suggests that in the startle response, the release of NE from the LC drives a coordinated increase in astrocytic [Ca2+]i in multiple brain regions. This suggests that coordinated astrocytic calcium transients in the awake brain are integrally related to widespread neuromodulation in response to behaviorally salient stimuli – placing them at the center of the network response to these stimuli.