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A cannabinoid type 2 receptor agonist attenuates blood-brain barrier damage and neurodegeneration in a murine model of traumatic brain injury.
J Neurosci Res 2012; 90(12):2293-305JN

Abstract

After traumatic brain injury (TBI), inflammation participates in both the secondary injury cascades and the repair of the CNS, both of which are influenced by the endocannabinoid system. This study determined the effects of repeated treatment with a cannabinoid type 2 receptor (CB(2) R) agonist on blood-brain barrier integrity, neuronal degeneration, and behavioral outcome in mice with TBI. We also looked for the presence of a prolonged treatment effect on the macrophage/microglial response to injury. C57BL/6 mice underwent controlled cortical impact (CCI) and received repeated treatments with a CB(2) R agonist, 0-1966, or vehicle. After euthanasia at 6 hr or 1, 2, 3, or 7 days postinjury, brains were removed for histochemical analysis. Blood-brain barrier permeability changes were evaluated by using sodium fluorescein (NaF). Perilesional degenerating neurons, injury volumes, and macrophage/microglia cells were quantified by stereological methods. Rota-rod and open-field testing were performed to evaluate motor function and natural exploratory behavior in mice. 0-1966 Treatment resulted in a significant reduction in NaF uptake and number of degenerating neurons compared with the vehicle-treated group. 0-1966-Treated mice demonstrated improvement on rota-rod and open-field testing compared with vehicle-treated mice. These changes in CCI mice treated with 0-1966 were associated with a prolonged reduction in macrophage/microglia cell counts. In conclusion, repeated treatments with a CB(2) R agonist, 0-1966, result in attenuated blood-brain barrier disruption and neuronal degeneration. In addition, repeated treatment with 0-1966 shows prolonged treatment effects on behavior and the macrophage/microglia cell response over several days.

Authors+Show Affiliations

Department of Neurological Surgery, Thomas Jefferson University Hospital, Philadelphia, Pennsylvania, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

22903455

Citation

Amenta, Peter S., et al. "A Cannabinoid Type 2 Receptor Agonist Attenuates Blood-brain Barrier Damage and Neurodegeneration in a Murine Model of Traumatic Brain Injury." Journal of Neuroscience Research, vol. 90, no. 12, 2012, pp. 2293-305.
Amenta PS, Jallo JI, Tuma RF, et al. A cannabinoid type 2 receptor agonist attenuates blood-brain barrier damage and neurodegeneration in a murine model of traumatic brain injury. J Neurosci Res. 2012;90(12):2293-305.
Amenta, P. S., Jallo, J. I., Tuma, R. F., & Elliott, M. B. (2012). A cannabinoid type 2 receptor agonist attenuates blood-brain barrier damage and neurodegeneration in a murine model of traumatic brain injury. Journal of Neuroscience Research, 90(12), pp. 2293-305. doi:10.1002/jnr.23114.
Amenta PS, et al. A Cannabinoid Type 2 Receptor Agonist Attenuates Blood-brain Barrier Damage and Neurodegeneration in a Murine Model of Traumatic Brain Injury. J Neurosci Res. 2012;90(12):2293-305. PubMed PMID: 22903455.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - A cannabinoid type 2 receptor agonist attenuates blood-brain barrier damage and neurodegeneration in a murine model of traumatic brain injury. AU - Amenta,Peter S, AU - Jallo,Jack I, AU - Tuma,Ronald F, AU - Elliott,Melanie B, Y1 - 2012/08/18/ PY - 2011/12/06/received PY - 2012/06/01/revised PY - 2012/06/14/accepted PY - 2012/8/21/entrez PY - 2012/8/21/pubmed PY - 2013/4/12/medline SP - 2293 EP - 305 JF - Journal of neuroscience research JO - J. Neurosci. Res. VL - 90 IS - 12 N2 - After traumatic brain injury (TBI), inflammation participates in both the secondary injury cascades and the repair of the CNS, both of which are influenced by the endocannabinoid system. This study determined the effects of repeated treatment with a cannabinoid type 2 receptor (CB(2) R) agonist on blood-brain barrier integrity, neuronal degeneration, and behavioral outcome in mice with TBI. We also looked for the presence of a prolonged treatment effect on the macrophage/microglial response to injury. C57BL/6 mice underwent controlled cortical impact (CCI) and received repeated treatments with a CB(2) R agonist, 0-1966, or vehicle. After euthanasia at 6 hr or 1, 2, 3, or 7 days postinjury, brains were removed for histochemical analysis. Blood-brain barrier permeability changes were evaluated by using sodium fluorescein (NaF). Perilesional degenerating neurons, injury volumes, and macrophage/microglia cells were quantified by stereological methods. Rota-rod and open-field testing were performed to evaluate motor function and natural exploratory behavior in mice. 0-1966 Treatment resulted in a significant reduction in NaF uptake and number of degenerating neurons compared with the vehicle-treated group. 0-1966-Treated mice demonstrated improvement on rota-rod and open-field testing compared with vehicle-treated mice. These changes in CCI mice treated with 0-1966 were associated with a prolonged reduction in macrophage/microglia cell counts. In conclusion, repeated treatments with a CB(2) R agonist, 0-1966, result in attenuated blood-brain barrier disruption and neuronal degeneration. In addition, repeated treatment with 0-1966 shows prolonged treatment effects on behavior and the macrophage/microglia cell response over several days. SN - 1097-4547 UR - https://www.unboundmedicine.com/medline/citation/22903455/A_cannabinoid_type_2_receptor_agonist_attenuates_blood_brain_barrier_damage_and_neurodegeneration_in_a_murine_model_of_traumatic_brain_injury_ L2 - https://doi.org/10.1002/jnr.23114 DB - PRIME DP - Unbound Medicine ER -