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Acute effects of a selective cannabinoid-2 receptor agonist on neuroinflammation in a model of traumatic brain injury.

Abstract

Proposed therapeutic strategies for attenuating secondary traumatic brain injury (TBI) include modulation of acute neuroimmune responses. The goal of this study was to examine the acute effects of cannabinoid-2 receptor (CB(2)R) modulation on behavioral deficits, cerebral edema, perivascular substance P, and macrophage/microglial activation in a murine model of TBI. Thirty male C57BL/6 mice underwent sham surgery, or cortical contusion impact injury (CCI). CCI mice received vehicle or the CB(2)R agonist 0-1966 at 1 and 24 h after injury. Performance on the rotarod, forelimb cylinder, and open-field tests were evaluated before and at 48 h after sham or CCI surgery. Cerebral edema was evaluated using the wet-dry weight technique. Immunohistochemical analysis was used to examine changes in substance P and macrophage/microglia-specific Iba1 protein immunoreactivity. Locomotor performance and exploratory behavior were significantly improved in mice receiving 0-1966 (CB(2)R agonist) compared to vehicle-treated mice. Significant reductions were found for cerebral edema, number of perivascular areas of substance P immunoreactivity, and number of activated macrophages/microglial cells in the injured brains of 0-1966-treated mice compared to vehicle-treated mice. The findings show that the effects of the CB(2)R agonist 0-1966 on edema, substance P immunoreactivity, and macrophage/microglial activation, were associated with recovery of acute motor and exploratory deficits. This study provides evidence of acute neuroprotective effects derived from selective CB(2)R activation that may represent an avenue for further development of novel therapeutic agents in the treatment of TBI.

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  • Publisher Full Text
  • Authors+Show Affiliations

    ,

    Department of Neurological Surgery, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA. melanie.elliott@jefferson.edu

    , , ,

    Source

    Journal of neurotrauma 28:6 2011 Jun pg 973-81

    MeSH

    Animals
    Anisoles
    Brain Injuries
    Cannabinoid Receptor Modulators
    Cyclohexanols
    Disease Models, Animal
    Inflammation
    Inflammation Mediators
    Male
    Mice
    Mice, Inbred C57BL
    Neurons
    Receptor, Cannabinoid, CB2
    Resorcinols

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    21332427

    Citation

    * When formatting your citation, note that all book, journal, and database titles should be italicized* Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Acute effects of a selective cannabinoid-2 receptor agonist on neuroinflammation in a model of traumatic brain injury. AU - Elliott,Melanie B, AU - Tuma,Ronald F, AU - Amenta,Peter S, AU - Barbe,Mary F, AU - Jallo,Jack I, Y1 - 2011/06/01/ PY - 2011/2/22/entrez PY - 2011/2/22/pubmed PY - 2012/5/15/medline SP - 973 EP - 81 JF - Journal of neurotrauma JO - J. Neurotrauma VL - 28 IS - 6 N2 - Proposed therapeutic strategies for attenuating secondary traumatic brain injury (TBI) include modulation of acute neuroimmune responses. The goal of this study was to examine the acute effects of cannabinoid-2 receptor (CB(2)R) modulation on behavioral deficits, cerebral edema, perivascular substance P, and macrophage/microglial activation in a murine model of TBI. Thirty male C57BL/6 mice underwent sham surgery, or cortical contusion impact injury (CCI). CCI mice received vehicle or the CB(2)R agonist 0-1966 at 1 and 24 h after injury. Performance on the rotarod, forelimb cylinder, and open-field tests were evaluated before and at 48 h after sham or CCI surgery. Cerebral edema was evaluated using the wet-dry weight technique. Immunohistochemical analysis was used to examine changes in substance P and macrophage/microglia-specific Iba1 protein immunoreactivity. Locomotor performance and exploratory behavior were significantly improved in mice receiving 0-1966 (CB(2)R agonist) compared to vehicle-treated mice. Significant reductions were found for cerebral edema, number of perivascular areas of substance P immunoreactivity, and number of activated macrophages/microglial cells in the injured brains of 0-1966-treated mice compared to vehicle-treated mice. The findings show that the effects of the CB(2)R agonist 0-1966 on edema, substance P immunoreactivity, and macrophage/microglial activation, were associated with recovery of acute motor and exploratory deficits. This study provides evidence of acute neuroprotective effects derived from selective CB(2)R activation that may represent an avenue for further development of novel therapeutic agents in the treatment of TBI. SN - 1557-9042 UR - https://www.unboundmedicine.com/medline/citation/21332427/abstract/Acute_effects_of_a_selective_cannabinoid_2_receptor_agonist_on_neuroinflammation_in_a_murine_model_of_traumatic_brain_injury_ L2 - https://www.liebertpub.com/doi/full/10.1089/neu.2010.1672?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -