Specific features of visual objects innately draw approach responses in animals, and provide natural signals of potential reward. However, visual sampling behaviours and the detection of salient, rewarding stimuli are context and behavioural state-dependent and it remains unclear how visual perception and orienting responses change with specific expectations. To start to address this question, we employed a virtual stimulus orienting paradigm based on prey capture to quantify the conditional expression of visual stimulus-evoked innate approaches in freely moving mice. We found that specific combinations of stimulus features selectively evoked innate approach or freezing responses when stimuli were unexpected. We discovered that prey capture experience, and therefore the expectation of prey in the environment, selectively modified approach frequency, as well as altered those visual features that evoked approach. Thus, we found that mice exhibit robust and selective orienting responses to parameterized visual stimuli that can be robustly and specifically modified via natural experience. This work provides critical insight into how natural appetitive behaviours are driven by both specific features of visual motion and internal states that alter stimulus salience.
Bimanual coordination is governed by constraints that permit congruent movements to be performed more easily than incongruent movements. Theories concerning the origin of these constraints range from low level motor-muscle explanations to high level perceptual-cognitive ones. To elucidate the processes underlying coordinative constraints, we asked subjects to use a pair of left-right joysticks to acquire corresponding pairs of congruent and incongruent targets presented on a video monitor under task conditions designed to systematically modulate the impact of several perceptual-cognitive processes commonly required for bimanual task performance. These processes included decoding symbolic cues, detecting goal targets, conceptualizing movements in terms of goal target configuration, planning movement trajectories, producing saccades and perceiving visual feedback. Results demonstrate that constraints arise from target detection and trajectory planning processes that can occur prior to movement initiation as well as from inherent muscle properties that emerge during movement execution, and that the manifestation of these constraints can be significantly altered by the ability to visually monitor movement progress.
Non-myelinating Schwann cells (NMSC) play important roles in peripheral nervous system formation and function. However, the molecular identity of these cells remains poorly defined. We provide evidence that Kir4.1, an inward-rectifying K+ channel encoded by the KCNJ10 gene, is specifically expressed and active in NMSC.Immunostaining revealed that Kir4.1 is present in terminal/perisynaptic SCs (TPSC), synaptic glia at neuromuscular junctions (NMJ), but not in myelinating SCs (MSC) of adult mice. To further examine the expression pattern of Kir4.1, we generated BAC transgenic Kir4.1-CreER T2 mice and crossed them to the tdTomato reporter line. Activation of CreER T2 with tamoxifen after the completion of myelination onset led to robust expression of tdTomato in NMSC, including Remak Schwann cells (RSC) along peripheral nerves and TPSC, but not in MSC. In contrast, activating CreER T2 before and during the onset of myelination led to tdTomato expression in NMSC and MSC.These observations suggest that immature SC express Kir4.1, and its expression is then downregulated selectively in myelin-forming SC. In support, we found that while activating CreER T2 induces tdTomato expression in immature SC, it fails to induce tdTomato in MSC associated with sensory axons in culture. NMSC derived from neonatal sciatic nerve were shown to express Kir4.1 and exhibit barium-sensitive inwardly rectifying macroscopic K + currents. Thus, this study identified Kir4.1 as a potential modulator of immature SC and NMSC function. Additionally, it established a novel transgenic mouse line to introduce or delete genes in NMSC.
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