Cholinergic input to mouse visual cortex signals a movement state and acutely enhances layer 5 responsiveness.

Acetylcholine is released in visual cortex by axonal projections from the basal forebrain. The signals conveyed by these projections and their computational significance are still unclear. Using two-photon calcium imaging in behaving mice, we show that basal forebrain cholinergic axons in the mouse visual cortex provide a binary locomotion state signal. In these axons, we found no evidence of responses to visual stimuli or visuomotor prediction errors. While optogenetic activation of cholinergic axons in visual cortex in isolation did not drive local neuronal activity, when paired with visuomotor stimuli, it resulted in layer-specific increases of neuronal activity. Responses in layer 5 neurons to both top-down and bottom-up inputs were increased in amplitude and decreased in latency, whereas those in layer 2/3 neurons remained unchanged. Using opto- and chemogenetic manipulations of cholinergic activity, we found acetylcholine to underlie the locomotion-associated decorrelation of activity between neurons in both layer 2/3 and layer 5. Our results suggest that acetylcholine augments the responsiveness of layer 5 neurons to inputs from outside of the local network, possibly enabling faster switching between internal representations during locomotion.

Retinoic acid signaling regulates proliferation and lamina formation in the developing chick optic tectum.

The retinotectal system has been extensively studied for investigating the mechanism(s) for topographic map formation. The optic tectum, which is composed of multiple laminae, is the major retino recipient structure in the developing avian brain. Laminar development of the tectum results from cell proliferation, differentiation and migration, coordinated in strict temporal and spatial patterns. However, the molecular mechanisms that orchestrate these complex developmental events, have not been fully elucidated. In this study, we have identified the presence of differential retinoic acid (RA) signaling along the rostro-caudal and dorsoventral axis of the tectum. We show for the first time that loss of RA signaling in the anterior optic tectum, leads to an increase in cell proliferation and gross changes in the morphology manifested as defects in lamination. Detailed analysis points to delayed migration of cells as the plausible cause for the defects in lamina formation. Thus, we conclude that in the optic tectum, RA signaling is involved in maintaining cell proliferation and in regulating the formation of the tectal laminae.