Excitatory amino acid receptor subtype binding following traumatic brain injury.

Department of Psychology, Virginia Commonwealth University, Ричмонд, Virginia, United States
Brain Research (Impact Factor: 2.83). 09/1990; 526(1):103-7. DOI: 10.1016/0006-8993(90)90254-9
Source: PubMed

ABSTRACT Sprague-Dawley rats were subjected to a moderate level (2.2 atm) of traumatic brain injury (TBI) using fluid percussion. Injured animals were allowed post-trauma survival periods of 5 min, 3 and 24 h. Regional glutamate receptor subtype binding was assessed with quantitative autoradiography in each group for N-methyl-D-aspartate (NMDA), quisqualate and kainate receptor subpopulations at approximately the -3.8 bregma level and compared to a sham control group. [3H]glutamate binding to the NMDA receptor was significantly (P less than 0.05) decreased at 3 h post-TBI in the hippocampal CA1 stratum radiatum, the molecular layers of the dentate gyri and the outer (layers 1-3) and inner (layers 5 and 6) overlying neocortex. NMDA receptor binding was significantly reduced in layers 5 and 6 of the neocortex at all post-trauma survival times but no further differences were seen in the hippocampi. No significant changes were observed with [3H]AMPA binding to quisqualate receptors and [3H]KA binding was significantly reduced only in layers 5 and 6 of the neocortex at 24 h after TBI. These data further confirm the pathological involvement of the NMDA receptor complex in brain regions selectively vulnerable to moderate levels of TBI in this model.

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Traumatic brain injury (TBI) is a leading cause of morbidity and mortality in the United States, and the incidence has been increasing within the geriatric age group as the population ages. There are many factors that are unique to this subgroup, including normal aging processes, differences in pathophysiology, and inherent medical comorbidities that affect their outcomes, treatment, and therefore, the allocation of medical and social services. The geriatric population has age-appropriate strength, coordination and balance deficits that make them predisposed to falls and subsequent TBI. The aging brain often has premorbid atrophy and increased susceptibility to the inflammatory, excitatory, and vascular processes that facilitate neurologic damage during the acute phases after injury. The aged also can have premorbid neurodegenerative and medical comorbidities that also affect their rehabilitation course, recovery, and outcomes once a TBI has occurred. Pharmacological strategies to maximize rehabilitation and recovery require specific considerations of the potential for adverse effects and contraindications specific to common comorbidities in the aged population. The management of geriatric TBI requires a coordinated effort between physicians and other healthcare providers with focus on risk factor modification, medical optimization, and successful return to the community by setting goals that emphasize level of function and quality of life.
    09/2012; 1(3). DOI:10.1007/s13670-012-0021-6
  • Neural Regeneration Research 06/2014; 9(11):1093-5. DOI:10.4103/1673-5374.135306 · 0.23 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Traumatic brain injury (TBI) induces glutamatergic excitotoxicity through N-methyl-D-aspartate (NMDA) receptors, affecting the integrity of the mitochondrial membrane. Studies have pointed to mitochondria as the master organelle in the preconditioning-triggered endogenous neuroprotective response. The present study is aimed at understanding energy metabolism in the brains of mice after preconditioning with NMDA and TBI. For this purpose, male albino CF-1 mice were pre-treated with NMDA (75 mg/kg) and subjected to brain trauma. Mitochondrial respiratory chain and creatine kinase activities were assessed at 6 or 24 h after trauma. The mice preconditioned and subjected to TBI exhibited augmented activities of complexes II and IV in the cerebral cortex and/or cerebellum. Creatine kinase activity was also augmented in the cerebral cortex after 24 h. We suggest that even though NMDA preconditioning and TBI have similar effects on enzyme activities, each manage their response via opposite mechanisms because the protective effects of preconditioning are unambiguous. In conclusion, NMDA preconditioning induces protection via an increase of enzymes in the mitochondria.
    Molecular and Cellular Biochemistry 09/2013; 384(1-2). DOI:10.1007/s11010-013-1790-8 · 2.39 Impact Factor