SummaryThe neural circuits underlying goal-directed sensorimotor transformations in the mammalian brain are incompletely understood. Here, we compared the role of primary tongue-jaw motor cortex (tjM1) and primary whisker sensory cortex (wS1) in head-restrained mice trained to lick a reward spout in response to whisker deflection. Two-photon microscopy combined with microprisms allowed imaging of neuronal network activity across cortical layers in transgenic mice expressing a genetically encoded calcium indicator. Early-phase activity in wS1 encoded the whisker sensory stimulus and was necessary for detection of whisker stimuli. Activity in tjM1 encoded licking direction during task execution and was necessary for contralateral licking. Pre-stimulus activity in tjM1, but not wS1, was predictive of lick direction and contributed causally to small preparatory jaw movements. Our data reveal a shift in coding scheme from wS1 to tjM1, consistent with the hypothesis that these areas represent cortical start and end points for this goal-directed sensorimotor transformation.

Abstract. Sensorimotor processing occurs in a highly distributed manner in the mammalian neocortex. The spatiotemporal dynamics of electrical activity in the dorsal mouse neocortex can be imaged using voltagesensitive dyes (VSDs) with near-millisecond temporal resolution and ∼100-μm spatial resolution. Here, we trained mice to lick a water reward spout after a 1-ms deflection of the C2 whisker, and we imaged cortical dynamics during task execution with VSD RH1691. Responses to whisker deflection were highly dynamic and spatially highly distributed, exhibiting high variability from trial to trial in amplitude and spatiotemporal dynamics. We differentiated trials based on licking and whisking behavior. Hit trials, in which the mouse licked after the whisker stimulus, were accompanied by overall greater depolarization compared to miss trials, with the strongest hit versus miss differences being found in frontal cortex. Prestimulus whisking decreased behavioral performance by increasing the fraction of miss trials, and these miss trials had attenuated cortical sensorimotor responses. Our data suggest that the spatiotemporal dynamics of depolarization in mouse sensorimotor cortex evoked by a single brief whisker deflection are subject to important behavioral modulation during the execution of a simple, learned, goal-directed sensorimotor transformation.

HighlightsOptogenetic whisker motor mapping in awake head-restrained mice.Stimulation of whisker sensory cortex evokes contralateral whisker retraction.Stimulation of frontal cortex evokes bilateral rhythmic whisker protraction.Stimulation of posteriomedial cortex evokes bilateral rhythmic whisker protraction.

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The ability of Mn 2? to follow Ca 2? pathways upon stimulation transform them into remarkable surrogate markers of neuronal activity using activity-induced manganese-dependent MRI (AIM-MRI). In the present study, a precise follow-up of physiological parameters during MnCl 2 and mannitol infusions improved the reproducibility of AIM-MRI allowing in-depth evaluation of the technique. Pixel-by-pixel T 1 data were investigated using histogram distributions in the barrel cortex (BC) and the thalamus before and after Mn 2? infusion, after blood brain barrier opening and after BC activation. Mean BC T 1 values dropped significantly upon trigeminal nerve (TGN) stimulation (-38 %, P = 0.02) in accordance with previous literature findings. T 1 histogram distributions showed that 34 % of T 1s in the range 600-1500 ms after Mn 2? ? mannitol infusions shifted to 50-350 ms after TGN stimulation corresponding to a twofold increase of the percentage of pixels with the lowest T 1s in BC. Moreover, T 1 changes in response to stimulation increased significantly from superficial cortical layers (I-III) to deeper layers (V-VI). Cortical cytoarchitecture detection during a functional paradigm was performed extending the potential of AIM-MRI. Quantitative AIM-MRI could thus offer a means to interpret local neural activity across cortical layers while identification of the role of calcium dynamics in vivo during brain activation could play a key role in resolving neurovascular coupling mechanisms.