title: Structural and functional effects of social isolation on the hippocampus of rats with traumatic brain injury.
abstract: Social isolation has significant long-term psychological and physiological consequences. Both social isolation and traumatic brain injury (TBI) alter normal brain function and structure. However, the influence of social isolation on recovery from TBI is unclear. This study aims to evaluate if social isolation exacerbates the anatomical and functional deficits after TBI in young rats. Juvenile male rats were divided into four groups; sham operated control with social contacts, sham control with social isolation, TBI with social contacts, and TBI with social isolation. During four weeks after brain injury in juvenile rats, we evaluated the animal behaviors by T-maze and open-field tests, recorded brain activity with electrocorticograms and assessed structural changes by histological procedures in the hippocampal dentate gyrus, CA1, and CA3 areas. Our findings revealed significant memory impairments and hyperactivity conditions in rats with TBI and social isolation compared to the other groups. Histological assessments showed an increase of the mean number of dark neurons, apoptotic cells, and caspase-3 positive cells in all tested areas of the hippocampus in TBI rats with and without social isolation compared to sham rats. Furthermore, social isolation significantly increased the number of dark cells, apoptotic neurons, and caspase-3 positive cells in the hippocampal CA3 region in rats with TBI. This study indicates the harmful effect of social isolation on anatomical and functional deficits induced by TBI in juvenile rats. Prevention of social isolation may improve the outcome of TBI.
authors.affiliation: Shefa Neuroscience Research Center, Khatam Hospital, Tehran, Iran; Faculty of Veterinary Medicine, Islamic Azad University Karaj Branch, Karaj, Iran.
authors.forename: Babak
authors.initials: B
authors.lastname: Khodaie
authors.affiliation: Shefa Neuroscience Research Center, Khatam Hospital, Tehran, Iran; Faculty of Veterinary Medicine, Islamic Azad University Karaj Branch, Karaj, Iran.
authors.forename: Ahmad Ali
authors.initials: AA
authors.lastname: Lotfinia
authors.affiliation: Shefa Neuroscience Research Center, Khatam Hospital, Tehran, Iran; Faculty of Veterinary Medicine, Islamic Azad University Karaj Branch, Karaj, Iran.
authors.forename: Milad
authors.initials: M
authors.lastname: Ahmadi
authors.affiliation: Shefa Neuroscience Research Center, Khatam Hospital, Tehran, Iran; Medical School of Shahid-Beheshti Medical University, Tehran, Iran.
authors.forename: Mahmoud
authors.initials: M
authors.lastname: Lotfinia
authors.affiliation: Shefa Neuroscience Research Center, Khatam Hospital, Tehran, Iran.
authors.forename: Maryam
authors.initials: M
authors.lastname: Jafarian
authors.affiliation: Shefa Neuroscience Research Center, Khatam Hospital, Tehran, Iran.
authors.forename: Fariba
authors.initials: F
authors.lastname: Karimzadeh
authors.affiliation: Epilepsy Research Center.
authors.forename: Philippe
authors.initials: P
authors.lastname: Coulon
authors.affiliation: Shefa Neuroscience Research Center, Khatam Hospital, Tehran, Iran; Epilepsy Research Center; Klinik und Poliklinik für Neurochirurgie; Department of Neurology; Institute of Neurophysiology, Westfälische Wilhelms-Universität Münster, Germany. Electronic address: gorjial@uni-muenster.de.
authors.forename: Ali
authors.initials: A
authors.lastname: Gorji
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001930:Brain Injuries / Q000473:pathology*; D058256:Brain Waves / Q000502:physiology*; D053148:Caspase 3 / Q000378:metabolism; D002452:Cell Count; D000069280:Electrocorticography; D005106:Exploratory Behavior; D006624:Hippocampus / Q000473:pathology* / Q000503:physiopathology*; D020287:In Situ Nick-End Labeling; D008297:Male; D018782:Maze Learning / Q000502:physiology; D009416:Nerve Regeneration / Q000502:physiology; D009474:Neurons / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D012934:Social Isolation; D013997:Time Factors
chemical_list: D053148:Caspase 3
keywords: Brain trauma; Cell death; Cognition; Memory impairment; Neuronal damage