Decoding Hippocampal Signaling Deficits After Traumatic Brain Injury
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REVIEW ARTICLE
Decoding Hippocampal Signaling Deficits After Traumatic Brain Injury Coleen M. Atkins
Received: 1 August 2011 / Revised: 17 October 2011 / Accepted: 24 October 2011 / Published online: 10 November 2011 # Springer Science+Business Media, LLC 2011
Abstract There are more than 3.17 million people coping with long-term disabilities due to traumatic brain injury (TBI) in the United States. The majority of TBI research is focused on developing acute neuroprotective treatments to prevent or minimize these long-term disabilities. Therefore, chronic TBI survivors represent a large, underserved population that could significantly benefit from a therapy that capitalizes on the endogenous recovery mechanisms occurring during the weeks to months following brain trauma. Previous studies have found that the hippocampus is highly vulnerable to brain injury, in both experimental models of TBI and during human TBI. Although often not directly mechanically injured by the head injury, in the weeks to months following TBI, the hippocampus undergoes atrophy and exhibits deficits in long-term potentiation (LTP), a persistent increase in synaptic strength that is considered to be a model of learning and memory. Decoding the chronic hippocampal LTP and cell signaling deficits after brain trauma will provide new insights into the molecular mechanisms of hippocampal-dependent learning impairments caused by TBI and facilitate the development of effective therapeutic strategies to improve hippocampaldependent learning for chronic survivors of TBI. Keywords Learning . Long-term potentiation . Memory . Protein kinase . Synapse . Traumatic brain injury
C. M. Atkins (*) Miami Project to Cure Paralysis, Department of Neurological Surgery, University of Miami Miller School of Medicine, PO Box 016960 (R-48), Miami, FL 33136, USA e-mail: [email protected]
Introduction Over 1.7 million people sustain a traumatic brain injury (TBI) every year in the United States, and 124,000 remain permanently disabled [1]. The resulting economic burden is approximately $56.3 billion per year [2]. An incident that takes only a second to occur can result in lifelong devastating consequences. People who have had a TBI are 1.8 times likely to report subsequent binge drinking, 1.5 times likely to be depressed, 2.3–4.5 times likely to develop Alzheimer’s, 7.5 times likely to die, and 29 times more likely to develop epilepsy [3–7]. Not only are there great personal costs, but there are also profound negative societal consequences; for example, an estimated 87% of prison inmates have incurred a head injury in their lifetime [8]. The neurological and behavioral sequelae of TBI develop over the course of days to months after the initial trauma. Most behavioral recovery is observed during the first 6 months after injury [9]. However, this recovery often plateaus or declines between 6 to 12 months after the TBI [10]. Although there are endogenous reparative mechanisms, these are simply not sufficient to achieve full recovery for most people with moderate to
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