Zoology - Research Publications

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    Role of Neurons and Glia Cells in Wound Healing as a Novel Perspective Considering Platelet as a Conventional Player
    (Springer, 2021-10-11T00:00:00) Beura, Samir K.; Panigrahi, Abhishek R.; Yadav, Pooja; Agrawal, Siwani; Singh, Sunil K.
    Wound healing is a complex physiological process in which the damaged or injured tissue is replaced or regenerated by new cells or existing cells respectively in their synthesized and secreted matrices. Several cells modulate the process of wound healing including macrophages, fibroblasts, and keratinocytes. Apart from these cells, platelet has been considered as a major cellular fragment to be involved in wound healing at several stages by secreting its granular contents including growth factors, thus resulting in coagulation, inflammation, and angiogenesis. A distant cell, which is gaining significant attention nowadays due to its resemblance with platelet in several aspects, is the neuron. Not only neurons but also glia cells are also confirmed to regulate wound healing at different stages in an orchestrated manner. Furthermore, these neurons and glia cells mediate wound healing inducing tissue repair and regeneration apart from hemostasis, angiogenesis, and inflammation by secreting various growth factors, coagulation molecules, immunomodulatory molecules as well as neurohormones, neuropeptides, and neurotrophins. Therefore, in wound healing platelets, neurons and glia cells not only contribute to tissue repair but are also responsible for establishing the wound microenvironment, thus affecting the proliferation of immune cells, fibroblast, and keratinocytes. Here in this review, we will enlighten the physiological roles of neurons and glia cells in coordination with platelets to understand various cellular and molecular mechanism in brain injury and associated neurocognitive impairments. � 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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    Dopamine, sleep, and neuronal excitability modulate amyloid-?-mediated forgetting in Drosophila
    (Public Library of Science, 2021-10-07T00:00:00) Kaldun, Jenifer C.; Lone, Shahnaz R.; Humbert Camps, Ana M.; Fritsch, Cornelia; Widmer, Yves F.; Stein, Jens V.; Tomchik, Seth M.; Sprecher, Simon G.
    Alzheimer disease (AD) is one of the main causes of age -related dementia and neurodegeneration. However, the onset of the disease and the mechanisms causing cognitive defects are not well understood. Aggregation of amyloidogenic peptides is a pathological hallmark of AD and is assumed to be a central component of the molecular disease pathways. Panneuronal expression of A?42 Arctic peptides in Drosophila melanogaster results in learning and memory defects. Surprisingly, targeted expression to the mushroom bodies, a center for olfactory memories in the fly brain, does not interfere with learning but accelerates forgetting. We show here that reducing neuronal excitability either by feeding Levetiracetam or silencing of neurons in the involved circuitry ameliorates the phenotype. Furthermore, inhibition of the Rac-regulated forgetting pathway could rescue the A?42 Arctic-mediated accelerated forgetting phenotype. Similar effects are achieved by increasing sleep, a critical regulator of neuronal homeostasis. Our results provide a functional framework connecting forgetting signaling and sleep, which are critical for regulating neuronal excitability and homeostasis and are therefore a promising mechanism to modulate forgetting caused by toxic A? peptides. � 2021 Kaldun et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.