The release of acetylcholine (ACh) into the primary visual cortex (V1) following the activation of nucleus basalis modulates attention and is hypothesized to improve information processing via muscarinic receptor (mAChR) mediated mechanisms. Previously it has been demonstrated that visual cortex astrocytes in vivo respond with calcium elevations to visual stimuli and show tuned responses (Schummers et al., Science 320: 1638, 2008). Although several studies have focused on cholinergic effects on cortical neurons, the consequences of ACh on other cell types, such as astrocytes, are poorly understood. Here, we have investigated possible cholinergic-mediated signaling in cortical astrocytes and the consequential downstream effects on neurons. Using calcium imaging, whole cell patch-clamp and post-experimental immunohistochemistry, we screened for cholinergic responses of both neurons and astrocytes in the superficial layers of mouse V1 cortical slices. Local application of ACh induced intracellular calcium elevations in astrocytes, which were manifested by an increase in the frequency of TTX-insensitive calcium oscillations. These responses were abolished in the presence of atropine, an mAChR antagonist. On the other hand, cortical neurons displayed an increase in spontaneous low-frequency slow inward currents (SICs) that were abolished by AP5, an NMDA glutamatergic receptor antagonist. These results indicate that astrocytes are cellular targets of ACh, where their cholinergic excitation may modulate neuronal excitability via glutamate release.

Society for Neuroscience Abstract, 2010.