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  1. Artikel ; Online: Conditional Astrocyte Rac1KO Attenuates Hyperreflexia after Spinal Cord Injury.

    Benson, Curtis A / Olson, Kai-Lan / Patwa, Siraj / Kauer, Sierra D / King, Jared F / Waxman, Stephen G / Tan, Andrew M

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2024  Band 44, Heft 1

    Abstract: Spasticity is a hyperexcitability disorder that adversely impacts functional recovery and rehabilitative efforts after spinal cord injury (SCI). The loss of evoked rate-dependent depression (RDD) of the monosynaptic H-reflex is indicative of ... ...

    Abstract Spasticity is a hyperexcitability disorder that adversely impacts functional recovery and rehabilitative efforts after spinal cord injury (SCI). The loss of evoked rate-dependent depression (RDD) of the monosynaptic H-reflex is indicative of hyperreflexia, a physiological sign of spasticity. Given the intimate relationship between astrocytes and neurons, that is, the tripartite synapse, we hypothesized that astrocytes might have a significant role in post-injury hyperreflexia and plasticity of neighboring neuronal synaptic dendritic spines. Here, we investigated the effect of selective Rac1KO in astrocytes (i.e., adult male and female mice, transgenic cre-flox system) on SCI-induced spasticity. Three weeks after a mild contusion SCI, control Rac1
    Mesh-Begriff(e) Mice ; Male ; Female ; Animals ; Reflex, Abnormal ; Astrocytes/metabolism ; Spinal Cord Injuries ; Motor Neurons/physiology ; Spinal Cord/metabolism ; Animals, Genetically Modified ; H-Reflex ; Amino Acid Transport System X-AG/metabolism
    Chemische Substanzen Amino Acid Transport System X-AG
    Sprache Englisch
    Erscheinungsdatum 2024-01-03
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.1670-22.2023
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Cell death in development, maintenance, and diseases of the nervous system

    Mercau, Maria E. / Patwa, Siraj / Bhat, Krishna P. L. / Ghosh, Sourav / Rothlin, Carla V.

    Semin Immunopathol. 2022 Sept., v. 44, no. 5, p. 725-738

    2022  , Seite(n) 725–738

    Abstract: Cell death, be it of neurons or glial cells, marks the development of the nervous system. Albeit relatively less so than in tissues such as the gut, cell death is also a feature of nervous system homeostasis—especially in context of adult neurogenesis. ... ...

    Abstract Cell death, be it of neurons or glial cells, marks the development of the nervous system. Albeit relatively less so than in tissues such as the gut, cell death is also a feature of nervous system homeostasis—especially in context of adult neurogenesis. Finally, cell death is commonplace in acute brain injuries, chronic neurodegenerative diseases, and in some central nervous system tumors such as glioblastoma. Recent studies are enumerating the various molecular modalities involved in the execution of cells. Intimately linked with cell death are mechanisms of disposal that remove the dead cell and bring about a tissue-level response. Heretofore, the association between these methods of dying and physiological or pathological responses has remained nebulous. It is envisioned that careful cartography of death and disposal may reveal novel understandings of disease states and chart new therapeutic strategies in the near future.
    Schlagwörter adults ; brain ; cartography ; cell death ; death ; digestive system ; glioblastoma ; neurogenesis ; therapeutics
    Sprache Englisch
    Erscheinungsverlauf 2022-09
    Umfang p. 725-738
    Erscheinungsort Springer Berlin Heidelberg
    Dokumenttyp Artikel ; Online
    Anmerkung Review
    ZDB-ID 2316828-6
    ISSN 1863-2300 ; 1863-2297
    ISSN (online) 1863-2300
    ISSN 1863-2297
    DOI 10.1007/s00281-022-00938-4
    Datenquelle NAL Katalog (AGRICOLA)

    Volltext online

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  3. Artikel ; Online: Cell death in development, maintenance, and diseases of the nervous system.

    Mercau, Maria E / Patwa, Siraj / Bhat, Krishna P L / Ghosh, Sourav / Rothlin, Carla V

    Seminars in immunopathology

    2022  Band 44, Heft 5, Seite(n) 725–738

    Abstract: Cell death, be it of neurons or glial cells, marks the development of the nervous system. Albeit relatively less so than in tissues such as the gut, cell death is also a feature of nervous system homeostasis-especially in context of adult neurogenesis. ... ...

    Abstract Cell death, be it of neurons or glial cells, marks the development of the nervous system. Albeit relatively less so than in tissues such as the gut, cell death is also a feature of nervous system homeostasis-especially in context of adult neurogenesis. Finally, cell death is commonplace in acute brain injuries, chronic neurodegenerative diseases, and in some central nervous system tumors such as glioblastoma. Recent studies are enumerating the various molecular modalities involved in the execution of cells. Intimately linked with cell death are mechanisms of disposal that remove the dead cell and bring about a tissue-level response. Heretofore, the association between these methods of dying and physiological or pathological responses has remained nebulous. It is envisioned that careful cartography of death and disposal may reveal novel understandings of disease states and chart new therapeutic strategies in the near future.
    Mesh-Begriff(e) Adult ; Cell Death ; Homeostasis ; Humans ; Nervous System ; Neurogenesis/physiology ; Neurons
    Sprache Englisch
    Erscheinungsdatum 2022-05-04
    Erscheinungsland Germany
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2316828-6
    ISSN 1863-2300 ; 1863-2297
    ISSN (online) 1863-2300
    ISSN 1863-2297
    DOI 10.1007/s00281-022-00938-4
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

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    Verfügbar in ZB MED Köln/Königswinter

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  4. Artikel ; Online: Conditional RAC1 knockout in motor neurons restores H-reflex rate-dependent depression after spinal cord injury.

    Benson, Curtis A / Olson, Kai-Lan / Patwa, Siraj / Reimer, Marike L / Bangalore, Lakshmi / Hill, Myriam / Waxman, Stephen G / Tan, Andrew M

    Scientific reports

    2021  Band 11, Heft 1, Seite(n) 7838

    Abstract: A major complication with spinal cord injury (SCI) is the development of spasticity, a clinical symptom of hyperexcitability within the spinal H-reflex pathway. We have previously demonstrated a common structural motif of dendritic spine dysgenesis ... ...

    Abstract A major complication with spinal cord injury (SCI) is the development of spasticity, a clinical symptom of hyperexcitability within the spinal H-reflex pathway. We have previously demonstrated a common structural motif of dendritic spine dysgenesis associated with hyperexcitability disorders after injury or disease insults to the CNS. Here, we used an adeno-associated viral (AAV)-mediated Cre-Lox system to knockout Rac1 protein expression in motor neurons after SCI. Three weeks after AAV9-Cre delivery into the soleus/gastrocnemius of Rac1-"floxed" adult mice to retrogradely infect spinal alpha-motor neurons, we observed significant restoration of RDD and reduced H-reflex excitability in SCI animals. Additionally, viral-mediated Rac1 knockdown reduced presence of dendritic spine dysgenesis on motor neurons. In control SCI animals without Rac1 knockout, we continued to observe abnormal dendritic spine morphology associated with hyperexcitability disorder, including an increase in mature, mushroom dendritic spines, and an increase in overall spine length and spine head size. Taken together, our results demonstrate that viral-mediated disruption of Rac1 expression in ventral horn motor neurons can mitigate dendritic spine morphological correlates of neuronal hyperexcitability, and reverse hyperreflexia associated with spasticity after SCI. Finally, our findings provide evidence of a putative mechanistic relationship between motor neuron dendritic spine dysgenesis and SCI-induced spasticity.
    Mesh-Begriff(e) Animals ; Anterior Horn Cells/metabolism ; Dendritic Spines/metabolism ; Dependovirus/genetics ; Depression/genetics ; Depression/metabolism ; Disease Models, Animal ; Female ; Gene Knockout Techniques/methods ; H-Reflex/genetics ; Locomotion/genetics ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle Spasticity/metabolism ; Neuronal Plasticity/genetics ; Neuropeptides/genetics ; Neuropeptides/metabolism ; Spinal Cord Injuries/genetics ; Spinal Cord Injuries/metabolism ; rac1 GTP-Binding Protein/genetics ; rac1 GTP-Binding Protein/metabolism
    Chemische Substanzen Neuropeptides ; Rac1 protein, mouse ; rac1 GTP-Binding Protein (EC 3.6.5.2)
    Sprache Englisch
    Erscheinungsdatum 2021-04-09
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-021-87476-5
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Dendritic Spine Dynamics after Peripheral Nerve Injury: An Intravital Structural Study.

    Benson, Curtis A / Fenrich, Keith K / Olson, Kai-Lan / Patwa, Siraj / Bangalore, Lakshmi / Waxman, Stephen G / Tan, Andrew M

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2020  Band 40, Heft 22, Seite(n) 4297–4308

    Abstract: Neuropathic pain is an intractable medical condition with few or no options for effective treatment. Emerging evidence shows a strong structure-function relationship between dendritic spine dysgenesis and the presence of neuropathic pain. Postmortem ... ...

    Abstract Neuropathic pain is an intractable medical condition with few or no options for effective treatment. Emerging evidence shows a strong structure-function relationship between dendritic spine dysgenesis and the presence of neuropathic pain. Postmortem tissue analyses can only imply dynamic structural changes associated with injury-induced pain. Here, we profiled the
    Mesh-Begriff(e) Animals ; Dendritic Spines/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Microscopy, Fluorescence, Multiphoton ; Peripheral Nerve Injuries/pathology ; Peripheral Nerve Injuries/physiopathology ; Spinal Cord Dorsal Horn/pathology ; Spinal Cord Dorsal Horn/physiopathology
    Sprache Englisch
    Erscheinungsdatum 2020-05-05
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.2858-19.2020
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

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  6. Artikel ; Online: Spinal cord motor neuron plasticity accompanies second-degree burn injury and chronic pain.

    Patwa, Siraj / Benson, Curtis A / Dyer, Lauren / Olson, Kai-Lan / Bangalore, Lakshmi / Hill, Myriam / Waxman, Stephen G / Tan, Andrew M

    Physiological reports

    2019  Band 7, Heft 23, Seite(n) e14288

    Abstract: Burn injuries and associated complications present a major public health challenge. Many burn patients develop clinically intractable complications, including pain and other sensory disorders. Recent evidence has shown that dendritic spine neuropathology ...

    Abstract Burn injuries and associated complications present a major public health challenge. Many burn patients develop clinically intractable complications, including pain and other sensory disorders. Recent evidence has shown that dendritic spine neuropathology in spinal cord sensory and motor neurons accompanies central nervous system (CNS) or peripheral nervous system (PNS) trauma and disease. However, no research has investigated similar dendritic spine neuropathologies following a cutaneous thermal burn injury. In this retrospective investigation, we analyzed dendritic spine morphology and localization in alpha-motor neurons innervating a burn-injured area of the body (hind paw). To identify a molecular regulator of these dendritic spine changes, we further profiled motor neuron dendritic spines in adult mice treated with romidepsin, a clinically approved Pak1-inhibitor, or vehicle control at two postburn time points: Day 6 immediately after treatment, or Day 10 following drug withdrawal. In control treated mice, we observed an overall increase in dendritic spine density, including structurally mature spines with mushroom-shaped morphology. Pak1-inhibitor treatment reduced injury-induced changes to similar levels observed in animals without burn injury. The effectiveness of the Pak1-inhibitor was durable, since normalized dendritic spine profiles remained as long as 4 days despite drug withdrawal. This study is the first report of evidence demonstrating that a second-degree burn injury significantly affects motor neuron structure within the spinal cord. Furthermore, our results support the opportunity to study dendritic spine dysgenesis as a novel avenue to clarify the complexities of neurological disease following traumatic injury.
    Mesh-Begriff(e) Animals ; Burns/complications ; Burns/drug therapy ; Burns/physiopathology ; Chronic Pain/drug therapy ; Chronic Pain/etiology ; Chronic Pain/physiopathology ; Dendritic Spines/drug effects ; Dendritic Spines/metabolism ; Dendritic Spines/physiology ; Depsipeptides/pharmacology ; Depsipeptides/therapeutic use ; Female ; Hot Temperature ; Male ; Mice ; Mice, Inbred C57BL ; Motor Neurons/drug effects ; Motor Neurons/physiology ; Neuronal Plasticity ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Reflex ; Spinal Cord/drug effects ; Spinal Cord/physiopathology ; p21-Activated Kinases/antagonists & inhibitors
    Chemische Substanzen Depsipeptides ; Protein Kinase Inhibitors ; romidepsin (CX3T89XQBK) ; Pak1 protein, mouse (EC 2.7.11.1) ; p21-Activated Kinases (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2019-12-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.14288
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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