![]() ![]() Other behavioral parameters such as grooming, wet dog shake, eating, drinking and rearing were not significantly altered. Results: CSD significantly decreased locomotor activity, induced freezing behavior and immobility in freely behaving rats. All AD events began from barrel cortex (n=7). Skull was left intact and no head fixation was used, in order to eliminate the possibility of injury-induced events. Because any craniotomy preparation could bias the onset location of CSD, we performed a separate series of experiments in which a completely uniform stimulus (systemic anoxia) elicited AD. The identity of barrel and visual cortex was confirmed by generating whisker and visual OIS maps. Additional experiments with craniotomy extended 2 mm more laterally and exposing barrel cortex, S2, auditory cortex, primary and lateral secondary visual cortex showed an identical pattern (n=5). 80% of CSD events began in either barrel cortex or visual cortex (n=21). Wide field optical intrinsic signal imaging (OIS) allowed identification of the initial CSD focus. Results: We first used a large 4*4 mm craniotomy to expose a wide area (including motor, somatosensory, cingulate, retrosplenial, association, and visual cortex) to increasing concentrations (8-120 mM) of potassium until CSD was elicited. Intracellular adhesion molecule (ICAM) mRNA, and tumor necrosis factor-alpha (TNF-α) mRNA in vehicle and CB 2-treated groups were measured using qRT-PCR. Blood-brain-barrier (BBB) permeability was evaluated using sodium fluorescein (NaF) (BBB disruption is a possible mechanism contributing to sensitization). CGRP immunoreactive trigeminal ganglia cells and growth-associated protein (GAP-43) in the trigeminal nucleus caudalis (TNC) were determined using immunohistochemistry and western blot. Baseline and weekly periorbital and paw von Frey (mechanical) allodynia testing were performed for up to four weeks post-injury. Craniotomy and incision-only mice were included as controls. CCI was induced in wild-type and CB 2R knockout mice with and without treatment with the CB 2R agonists (JWH-133 or 0-1966), or a CB 2R antagonist (SR144528). Methods: A CB 2R agonist (JWH-133 at 1 mg/kg) was compared to a triptan (Sumatriptan), a CGRP antagonist (MK8825), and saline in a model of controlled cortical impact (CCI) injury. All subjects Allied Health Cardiology & Cardiovascular Medicine Dentistry Emergency Medicine & Critical Care Endocrinology & Metabolism Environmental Science General Medicine Geriatrics Infectious Diseases Medico-legal Neurology Nursing Nutrition Obstetrics & Gynecology Oncology Orthopaedics & Sports Medicine Otolaryngology Palliative Medicine & Chronic Care Pediatrics Pharmacology & Toxicology Psychiatry & Psychology Public Health Pulmonary & Respiratory Medicine Radiology Research Methods & Evaluation Rheumatology Surgery Tropical Medicine Veterinary Medicine Cell Biology Clinical Biochemistry Environmental Science Life Sciences Neuroscience Pharmacology & Toxicology Biomedical Engineering Engineering & Computing Environmental Engineering Materials Science Anthropology & Archaeology Communication & Media Studies Criminology & Criminal Justice Cultural Studies Economics & Development Education Environmental Studies Ethnic Studies Family Studies Gender Studies Geography Gerontology & Aging Group Studies History Information Science Interpersonal Violence Language & Linguistics Law Management & Organization Studies Marketing & Hospitality Music Peace Studies & Conflict Resolution Philosophy Politics & International Relations Psychoanalysis Psychology & Counseling Public Administration Regional Studies Religion Research Methods & Evaluation Science & Society Studies Social Work & Social Policy Sociology Special Education Urban Studies & Planning BROWSE JOURNALS ![]()
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