Brain Areas Active during Visual Perception of Biological Motion

AbstractTheories of vision posit that form and motion are represented by neural mechanisms segregated into functionally and anatomically distinct pathways. Using point-light animations of biological motion, we examine the extent to which form and motion pathways are mutually involved in perceiving figures depicted by the spatio-temporal integration of local motion components. Previous work discloses that viewing biological motion selectively activates a region on the posterior superior temporal sulcus (STSp). Here we report that the occipital and fusiform face areas (OFA and FFA) also contain neural signals capable of differentiating biological from nonbiological motion. EBA and LOC, although involved in perception of human form, do not contain neural signals selective for biological motion. Our results suggest that a network of distributed neural areas in the form and motion pathways underlie the perception of biological motion

fMR-Adaptation Reveals Invariant Coding of Biological Motion on the Human STS

Neuroimaging studies of biological motion perception have found a network of coordinated brain areas, the hub of which appears to be the human posterior superior temporal sulcus (STSp). Understanding the functional role of the STSp requires characterizing the response tuning of neuronal populations underlying the BOLD response. Thus far our understanding of these response properties comes from single-unit studies of the monkey anterior STS, which has individual neurons tuned to body actions, with a small population invariant to changes in viewpoint, position and size of the action being viewed. To measure for homologous functional properties on the human STS, we used fMR-adaptation to investigate action, position and size invariance. Observers viewed pairs of point-light animations depicting human actions that were either identical, differed in the action depicted, locally scrambled, or differed in the viewing perspective, the position or the size. While extrastriate hMT+ had neural signals indicative of viewpoint specificity, the human STS adapted for all of these changes, as compared to viewing two different actions. Similar findings were observed in more posterior brain areas also implicated in action recognition. Our findings are evidence for viewpoint invariance in the human STS and related brain areas, with the implication that actions are abstracted into object-centered representations during visual analysis

When shapes are more than shapes: perceptual, developmental, and neurophysiological basis for attributions of animacy and theory of mind

Among a variety of entities in their environment, what do humans consider alive or animate and how does this attribution of animacy promote development of more abstract levels of mentalizing? By decontextualizing the environment of bodily features, we review how physical movements give rise to perceived animacy in Heider-Simmel style animations. We discuss the developmental course of how perceived animacy shapes our interpretation of the social world, and specifically discuss when and how children transition from perceiving actions as goal-directed to attributing behaviors to unobservable mental states. This transition from a teleological stance, asserting a goal-oriented interpretation to an agent's actions, to a mentalistic stance allows older children to reason about more complex actions guided by hidden beliefs. The acquisition of these more complex cognitive behaviors happens developmentally at the same time neural systems for social cognition are coming online in young children. We review perceptual, developmental, and neural evidence to identify the joint cognitive and neural changes associated with when children begin to mentalize and how this ability is instantiated in the brain

Distinct Cerebellar regions for Body Motion Discrimination.

Abstract Visual processing of human movements is critical for adaptive social behavior. Cerebellar activations have been observed during biological motion discrimination in prior neuroimaging studies, and cerebellar lesions may be detrimental for this task. However, whether the cerebellum plays a causal role in biological motion discrimination has never been tested. Here, we addressed this issue in three different experiments by interfering with the posterior cerebellar lobe using transcranial magnetic stimulation (TMS) during a biological discrimination task. In Experiments 1 and 2, we found that TMS delivered at onset of the visual stimuli over the vermis (vermal lobule VI), but not over the left cerebellar hemisphere (left lobule VI/Crus I), interfered with participants' ability to distinguish biological from scrambled motion compared to stimulation of a control site (vertex). Interestingly, when stimulation was delivered at a later time point (300 ms after stimulus onset), participants performed worse when TMS was delivered over the left cerebellar hemisphere compared to the vermis and the vertex (Experiment 3). Our data show that the posterior cerebellum is causally involved in biological motion discrimination and suggest that different sectors of the posterior cerebellar lobe may contribute to the task at different time points

Prolonged Neuromodulation of Cortical Networks Following Low-Frequency rTMS and Its Potential for Clinical Interventions

Non-invasive brain stimulation safely induces persistent large-scale neural modulation in functionally connected brain circuits. Interruption models of repetitive transcranial magnetic stimulation (rTMS) capitalize on the acute impact of brain stimulation, which decays over minutes. However, rTMS also induces longer-lasting impact on cortical functions, evident by the use of multi-session rTMS in clinical population for therapeutic purposes. Defining the persistent cortical dynamics induced by rTMS is complicated by the complex balance of excitation and inhibition among functionally connected networks. Nonetheless, it is these neuronal dynamic responses that are essential for the development of new neuromodulatory protocols for translational applications. We will review evidence of prolonged changes of cortical response, tens of minutes following one session of low frequency rTMS over the cortex. We will focus on the different methods which resulted in prolonged behavioral and brain changes, such as the combination of brain stimulation techniques, and individually tailored stimulation protocols. We will also highlight studies which apply these methods in multi-session stimulation practices to extend stimulation impact into weeks and months. Our data and others’ indicate that delayed cortical dynamics may persist much longer than previously thought and have potential as an extended temporal window during which cortical plasticity may be enhanced

Canvass: a crowd-sourced, natural-product screening library for exploring biological space

NCATS thanks Dingyin Tao for assistance with compound characterization. This research was supported by the Intramural Research Program of the National Center for Advancing Translational Sciences, National Institutes of Health (NIH). R.B.A. acknowledges support from NSF (CHE-1665145) and NIH (GM126221). M.K.B. acknowledges support from NIH (5R01GM110131). N.Z.B. thanks support from NIGMS, NIH (R01GM114061). J.K.C. acknowledges support from NSF (CHE-1665331). J.C. acknowledges support from the Fogarty International Center, NIH (TW009872). P.A.C. acknowledges support from the National Cancer Institute (NCI), NIH (R01 CA158275), and the NIH/National Institute of Aging (P01 AG012411). N.K.G. acknowledges support from NSF (CHE-1464898). B.C.G. thanks the support of NSF (RUI: 213569), the Camille and Henry Dreyfus Foundation, and the Arnold and Mabel Beckman Foundation. C.C.H. thanks the start-up funds from the Scripps Institution of Oceanography for support. J.N.J. acknowledges support from NIH (GM 063557, GM 084333). A.D.K. thanks the support from NCI, NIH (P01CA125066). D.G.I.K. acknowledges support from the National Center for Complementary and Integrative Health (1 R01 AT008088) and the Fogarty International Center, NIH (U01 TW00313), and gratefully acknowledges courtesies extended by the Government of Madagascar (Ministere des Eaux et Forets). O.K. thanks NIH (R01GM071779) for financial support. T.J.M. acknowledges support from NIH (GM116952). S.M. acknowledges support from NIH (DA045884-01, DA046487-01, AA026949-01), the Office of the Assistant Secretary of Defense for Health Affairs through the Peer Reviewed Medical Research Program (W81XWH-17-1-0256), and NCI, NIH, through a Cancer Center Support Grant (P30 CA008748). K.N.M. thanks the California Department of Food and Agriculture Pierce's Disease and Glassy Winged Sharpshooter Board for support. B.T.M. thanks Michael Mullowney for his contribution in the isolation, elucidation, and submission of the compounds in this work. P.N. acknowledges support from NIH (R01 GM111476). L.E.O. acknowledges support from NIH (R01-HL25854, R01-GM30859, R0-1-NS-12389). L.E.B., J.K.S., and J.A.P. thank the NIH (R35 GM-118173, R24 GM-111625) for research support. F.R. thanks the American Lebanese Syrian Associated Charities (ALSAC) for financial support. I.S. thanks the University of Oklahoma Startup funds for support. J.T.S. acknowledges support from ACS PRF (53767-ND1) and NSF (CHE-1414298), and thanks Drs. Kellan N. Lamb and Michael J. Di Maso for their synthetic contribution. B.S. acknowledges support from NIH (CA78747, CA106150, GM114353, GM115575). W.S. acknowledges support from NIGMS, NIH (R15GM116032, P30 GM103450), and thanks the University of Arkansas for startup funds and the Arkansas Biosciences Institute (ABI) for seed money. C.R.J.S. acknowledges support from NIH (R01GM121656). D.S.T. thanks the support of NIH (T32 CA062948-Gudas) and PhRMA Foundation to A.L.V., NIH (P41 GM076267) to D.S.T., and CCSG NIH (P30 CA008748) to C.B. Thompson. R.E.T. acknowledges support from NIGMS, NIH (GM129465). R.J.T. thanks the American Cancer Society (RSG-12-253-01-CDD) and NSF (CHE1361173) for support. D.A.V. thanks the Camille and Henry Dreyfus Foundation, the National Science Foundation (CHE-0353662, CHE-1005253, and CHE-1725142), the Beckman Foundation, the Sherman Fairchild Foundation, the John Stauffer Charitable Trust, and the Christian Scholars Foundation for support. J.W. acknowledges support from the American Cancer Society through the Research Scholar Grant (RSG-13-011-01-CDD). W.M.W.acknowledges support from NIGMS, NIH (GM119426), and NSF (CHE1755698). A.Z. acknowledges support from NSF (CHE-1463819). (Intramural Research Program of the National Center for Advancing Translational Sciences, National Institutes of Health (NIH); CHE-1665145 - NSF; CHE-1665331 - NSF; CHE-1464898 - NSF; RUI: 213569 - NSF; CHE-1414298 - NSF; CHE1361173 - NSF; CHE1755698 - NSF; CHE-1463819 - NSF; GM126221 - NIH; 5R01GM110131 - NIH; GM 063557 - NIH; GM 084333 - NIH; R01GM071779 - NIH; GM116952 - NIH; DA045884-01 - NIH; DA046487-01 - NIH; AA026949-01 - NIH; R01 GM111476 - NIH; R01-HL25854 - NIH; R01-GM30859 - NIH; R0-1-NS-12389 - NIH; R35 GM-118173 - NIH; R24 GM-111625 - NIH; CA78747 - NIH; CA106150 - NIH; GM114353 - NIH; GM115575 - NIH; R01GM121656 - NIH; T32 CA062948-Gudas - NIH; P41 GM076267 - NIH; R01GM114061 - NIGMS, NIH; R15GM116032 - NIGMS, NIH; P30 GM103450 - NIGMS, NIH; GM129465 - NIGMS, NIH; GM119426 - NIGMS, NIH; TW009872 - Fogarty International Center, NIH; U01 TW00313 - Fogarty International Center, NIH; R01 CA158275 - National Cancer Institute (NCI), NIH; P01 AG012411 - NIH/National Institute of Aging; Camille and Henry Dreyfus Foundation; Arnold and Mabel Beckman Foundation; Scripps Institution of Oceanography; P01CA125066 - NCI, NIH; 1 R01 AT008088 - National Center for Complementary and Integrative Health; W81XWH-17-1-0256 - Office of the Assistant Secretary of Defense for Health Affairs through the Peer Reviewed Medical Research Program; P30 CA008748 - NCI, NIH, through a Cancer Center Support Grant; California Department of Food and Agriculture Pierce's Disease and Glassy Winged Sharpshooter Board; American Lebanese Syrian Associated Charities (ALSAC); University of Oklahoma Startup funds; 53767-ND1 - ACS PRF; PhRMA Foundation; P30 CA008748 - CCSG NIH; RSG-12-253-01-CDD - American Cancer Society; RSG-13-011-01-CDD - American Cancer Society; CHE-0353662 - National Science Foundation; CHE-1005253 - National Science Foundation; CHE-1725142 - National Science Foundation; Beckman Foundation; Sherman Fairchild Foundation; John Stauffer Charitable Trust; Christian Scholars Foundation)Published versionSupporting documentatio

Correction of fragile X syndrome in mice

SummaryFragile X syndrome (FXS) is the most common form of heritable mental retardation and the leading identified cause of autism. FXS is caused by transcriptional silencing of the FMR1 gene that encodes the fragile X mental retardation protein (FMRP), but the pathogenesis of the disease is unknown. According to one proposal, many psychiatric and neurological symptoms of FXS result from unchecked activation of mGluR5, a metabotropic glutamate receptor. To test this idea we generated Fmr1 mutant mice with a 50% reduction in mGluR5 expression and studied a range of phenotypes with relevance to the human disorder. Our results demonstrate that mGluR5 contributes significantly to the pathogenesis of the disease, a finding that has significant therapeutic implications for fragile X and related developmental disorders