• Neural disruptions underlying feeding, s

    From ScienceDaily@1:317/3 to All on Wed Feb 23 21:30:44 2022
    Neural disruptions underlying feeding, swallowing disorders in children identified
    Neuroscience team provides insight on early cellular interactions
    underlying cranial nerve development

    Date:
    February 23, 2022
    Source:
    Virginia Tech
    Summary:
    Scientists depict the early development of pain-sensing and
    movement- sensing neurons in the face and throat. The findings
    reveal a previously unexplored feature of brain and cranial nerve
    development underlying eating, swallowing, and speech.



    FULL STORY ========================================================================== Every time you chew, talk, yawn, or sense the zap of a toothache, cranial
    nerve cells are shuttling electrochemical signals to your brain. Some
    of these neurons detect pain, while others sense facial muscle movements
    or sensations in the skin.


    ==========================================================================
    Now, in a new study published in Disease Models & Mechanisms, Fralin
    Biomedical Research Institute at VTC scientists led by Anthony-Samuel
    LaMantia depict the early development of pain-sensing and movement-sensing neurons in the face and throat. The findings reveal a previously
    unexplored feature of brain and cranial nerve development underlying
    eating, swallowing, and speech.

    "We were able to show for the first time that this momentary interaction between two groups of cells plays a crucial role in regulating movement
    and pain-sensing innervation in the face," LaMantia, professor and
    director of the Fralin Biomedical Research Institute's Center for
    Neurobiology Research.

    The researchers examined early neural development in mice embryos with
    DiGeorge syndrome, a rare genetic disorder associated with neural and
    facial abnormalities. Like human patients born with DiGeorge, mice can
    carry the identical genetic mutation, providing an ideal model to study
    where development goes awry at the cellular and molecular level.

    Children born with DiGeorge commonly have trouble coordinating suckling
    and swallowing milk, a condition called pediatric dysphagia, but it's
    unclear how the mutation causes these functional abnormalities. While
    mouth, tongue, and throat movements involved in eating are controlled
    by motor neurons, mechanosensory neurons -- a subject of this study --
    detect and integrate movement signals to fine-tune the behavior. The
    study also evaluated pain- sensing neurons, or nociceptors, which monitor potentially harmful aspects of eating behavior, including excessive temperatures and irritants like capsaicin in hot peppers.

    LaMantia and his laboratory have been studying this syndrome to
    disentangle facets of cranial nerve development and oropharyngeal
    behaviors for a decade.



    ========================================================================== Based on their prior research, the scientists knew that on day nine of
    mouse embryo development, two groups of cells -- neural crest and placode
    cells - - needed to meet to begin blueprinting the facial nerve. They
    knew that in the syndromic mice, something went wrong at this stage of development that had deleterious behavioral consequences, but it needed
    further investigation.

    "Starting out, we weren't sure if these two groups of cells just weren't migrating together to meet in the proper place, or if they were in the
    right place at the right time, and just failed to communicate," LaMantia
    said. With this newly published data, LaMantia's lab now suspects the
    latter is true.

    Combining in vivo analysis and imaging to visualize a variety of molecular markers, the researchers found that neural crest cells were turning
    into pain- sensing neurons far too soon. This premature differentiation
    caused the quantity of placode cells, which become mechanosensory neurons,
    to increase relative to neural crest cells.

    This study builds on previous work by LaMantia's lab. Seven years ago, the researchers examined if the developing cranial nerve neurons were growing
    axons that met functional targets in the face, mouth, and throat. They
    found that compared with ordinary mice, the syndromic mice embryos lacked proper innervation -- the axons were shorter, misplaced, and disorganized.

    "Not only were the neurons confused about what they were supposed to do,
    their axons also didn't have precise destinations -- they just got lost," LaMantia said.

    In a follow-up study, LaMantia's lab identified key genes involved in regulating normal axonal growth in the cranial nerve. Remarkably, the researchers were able to restore ordinary cranial nerve growth in mice
    with DiGeorge syndrome by suppressing a specific gene.

    The new discovery reveals how changes in gene expression associated with DiGeorge syndrome destabilize sensory neuron growth by interrupting a
    key interaction between neural crest and placode cells. LaMantia's lab
    now aims to uncover the molecular signals that these cell groups need
    to assemble a healthy cranial nerve.

    "Now that we've identified the point of divergence where these functional oropharyngeal problems originate, our next step will be to understand the vocabulary these cells use to communicate with each other," LaMantia said.

    This research was funded in part by the Eunice Kennedy Shriver
    National Institute of Child Health and Human Development, part of the
    National Institutes of Health; and the Fralin Biomedical Research
    Institute. LaMantia is also a professor in the College of Science
    Department of Biological Sciences and in the Virginia Tech Carilion
    School of Medicine Department of Pediatrics.

    special promotion Explore the latest scientific research on sleep and
    dreams in this free online course from New Scientist -- Sign_up_now_>>> ========================================================================== Story Source: Materials provided by Virginia_Tech. Original written by
    Whitney Slightham.

    Note: Content may be edited for style and length.


    ========================================================================== Journal Reference:
    1. Beverly A. Karpinski, Thomas M. Maynard, Corey A. Bryan, Gelila
    Yitsege,
    Anelia Horvath, Norman H. Lee, Sally A. Moody, Anthony-Samuel
    LaMantia.

    Selective disruption of trigeminal sensory neurogenesis
    and differentiation in a mouse model of 22q11.2 deletion
    syndrome. Disease Models & Mechanisms, 2022; 15 (2) DOI:
    10.1242/dmm.047357 ==========================================================================

    Link to news story: https://www.sciencedaily.com/releases/2022/02/220223085804.htm

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