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Deep learning-based markerless tracking has revolutionized studies of animal behavior. Yet the generalizability of trained models tends to be limited, as new training data typically needs to be generated manually for each setup or visual environment. With each model trained from scratch, researchers track distinct landmarks and analyze the resulting kinematic data in idiosyncratic ways. Moreover, due to inherent limitations in manual annotation, only a sparse set of landmarks are typically labeled. To address these issues, we developed an approach, which we term GlowTrack, for generating orders of magnitude more training data, enabling models that generalize across experimental contexts. We describe: a) a high-throughput approach for producing hidden labels using fluorescent markers; b) a multi-camera, multi-light setup for simulating diverse visual conditions; and c) a technique for labeling many landmarks in parallel, enabling dense tracking. These advances lay a foundation for standardized behavioral pipelines and more complete scrutiny of movement. Deep learning-based models for tracking behavior are often constrained by manual annotation. Here, authors present GlowTrack, an approach using fluorescence to generate large and diverse training sets that improve model robustness and tracking coverage.

The precision of skilled movement depends on sensory feedback and its refinement by local inhibitory microcircuits. One specialized set of spinal GABAergic interneurons forms axo–axonic contacts with the central terminals of sensory afferents, exerting presynaptic inhibitory control over sensory–motor transmission. The inability to achieve selective access to the GABAergic neurons responsible for this unorthodox inhibitory mechanism has left unresolved the contribution of presynaptic inhibition to motor behaviour. We used Gad2 as a genetic entry point to manipulate the interneurons that contact sensory terminals, and show that activation of these interneurons in mice elicits the defining physiological characteristics of presynaptic inhibition. Selective genetic ablation of Gad2 -expressing interneurons severely perturbs goal-directed reaching movements, uncovering a pronounced and stereotypic forelimb motor oscillation, the core features of which are captured by modelling the consequences of sensory feedback at high gain. Our findings define the neural substrate of a genetically hardwired gain control system crucial for the smooth execution of movement. A population of spinal interneurons that form axo–axonic connections with the terminals of proprioceptive afferents are shown to mediate presynaptic inhibition; their ablation elicits harmonic oscillations during goal-directed forelimb movements, which can be modelled as the consequence of an increase in sensory feedback gain. How presynaptic inhibition ensures smooth limb movement Humans and other animals execute limb movements with a seemingly effortless precision that relies on sensory feedback and its refinement by inhibitory microcircuits. A new study identifies presynaptic inhibition in the spinal cord, a regulatory filter mediated by Gad2 -expressing GABAergic interneurons that form connections with the terminals of sensory afferents, as part of a hardwired gain control system crucial for the smooth execution of movement. Thomas Jessell and colleagues demonstrate that activation of Gad2 -expressing neurons inhibits neurotransmitter release from sensory afferents. Selective ablation of these neurons in mice causes pronounced oscillations during goal-directed forelimb reaching movements, a behaviour captured by a model of sensory feedback at high gain.

Mutations in the transcriptional regulator Mecp2 cause the severe X-linked neurodevelopmental disorder Rett syndrome (RTT). In this study, we investigate genes that function downstream of MeCP2 in cerebral cortex circuitry, and identify upregulation of Irak1 , a central component of the NF-κB pathway. We show that overexpression of Irak1 mimics the reduced dendritic complexity of Mecp2 -null cortical callosal projection neurons (CPN), and that NF-κB signalling is upregulated in the cortex with Mecp2 loss-of-function. Strikingly, we find that genetically reducing NF-κB signalling in Mecp2 -null mice not only ameliorates CPN dendritic complexity but also substantially extends their normally shortened lifespan, indicating broader roles for NF-κB signalling in RTT pathogenesis. These results provide new insight into both the fundamental neurobiology of RTT, and potential therapeutic strategies via NF-κB pathway modulation. Rett syndrome is a neurodevelopmental disorder caused by mutations in Mecp2 . Here the authors show that Mecp2 loss-of-function leads to upregulation of the NF-κB pathway, and that reducing NF-κB signalling ameliorates phenotypes of Mecp2 -null mice, thus offering a potential therapeutic strategy.

Neurons coordinate their activity to produce an astonishing variety of motor behaviors. Our present understanding of motor control has grown rapidly thanks to new methods for recording and analyzing populations of many individual neurons over time. In contrast, current methods for recording the nervous system’s actual motor output – the activation of muscle fibers by motor neurons – typically cannot detect the individual electrical events produced by muscle fibers during natural behaviors and scale poorly across species and muscle groups. Here we present a novel class of electrode devices (‘Myomatrix arrays’) that record muscle activity at unprecedented resolution across muscles and behaviors. High-density, flexible electrode arrays allow for stable recordings from the muscle fibers activated by a single motor neuron, called a ‘motor unit,’ during natural behaviors in many species, including mice, rats, primates, songbirds, frogs, and insects. This technology therefore allows the nervous system’s motor output to be monitored in unprecedented detail during complex behaviors across species and muscle morphologies. We anticipate that this technology will allow rapid advances in understanding the neural control of behavior and identifying pathologies of the motor system.

With recent investigation beginning to reveal the cortical and subcortical neuroanatomical correlates of humor appreciation, the present event-related functional MRI (fMRI) study was designed to elucidate sex-specific recruitment of these humor related networks. Twenty healthy subjects (10 females) underwent fMRI scanning while subjectively rating 70 verbal and nonverbal achromatic cartoons as funny or unfunny. Data were analyzed by comparing blood oxygenation-level-dependent signal activation during funny and unfunny stimuli. Males and females share an extensive humor-response strategy as indicated by recruitment of similar brain regions: both activate the temporal-occipital junction and temporal pole, structures implicated in semantic knowledge and juxtaposition, and the inferior frontal gyrus, likely to be involved in language processing. Females, however, activate the left prefrontal cortex more than males, suggesting a greater degree of executive processing and language-based decoding. Females also exhibit greater activation of mesolimbic regions, including the nucleus accumbens, implying greater reward network response and possibly less reward expectation. These results indicate sex-specific differences in neural response to humor with implications for sex-based disparities in the integration of cognition and emotion.

All individuals immediately regained some ability to walk with robotic support during stimulation, and most showed a considerable increase in their ability to bear weight and a sustained improvement in walking after five months of EES treatment and rehabilitation. The group had previously developed a machine-learning approach to analyse gene-expression data that enabled identification of the cell types that respond to a biological stimulus11. To determine whether these V2a neurons promote recovery of walking, the authors performed a set of experiments to examine the effects of silencing or activating the cells in mice.

Improved treatments for spinal-cord injury require both technological development and insights into the biology of recovery. High-resolution molecular maps of the nervous system are beginning to provide the latter. The biological mechanisms that underpin rehabilitation after paralysis.

Previous research and theory suggest that two stable personality dimensions, extroversion and neuroticism, differentially influence emotional reactivity to a variety of pleasurable phenomena. Here, we use event-related functional MRI to address the putative neural and behavioral associations between humor appreciation and the personality dimensions of introversion-extroversion and emotional stability-neuroticism. Our analysis showed extroversion to positively correlate with humor-driven blood oxygenation level-dependent signal in discrete regions of the right orbital frontal cortex, ventrolateral prefrontal cortex, and bilateral temporal cortices. Introversion correlated with increased activation in several regions, most prominently the bilateral amygdala. Although neuroticism did not positively correlate with any whole-brain activation, emotional stability (i.e., the inverse of neuroticism) correlated with increased activation in the mesocortical-mesolimbic reward circuitry encompassing the right orbital frontal cortex, caudate, and nucleus accumbens. Our findings tie together existing neurobiological studies of humor appreciation and are compatible with the notion that personality style plays a fundamental role in the neurobiological systems subserving humor appreciation.

Coordinating intricate motor circuits A split second late or a few inches off the mark, and few would remember. Instead, running with his back to the ball, Willie Mays extended his arm and placed his glove squarely under the 420-foot center field drive. The New York Giants win Game 1 of the 1954 World Series, and Mays, his glove, and “The Catch” earn their place in history.