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      Dentate Gyrus Proliferative Responses After Traumatic Brain Injury and Binge Alcohol in Adult Rats

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          Abstract

          Background:

          Traumatic brain injury is a significant public health issue that results in serious disability in survivors. Traumatic brain injury patients are often intoxicated with alcohol when admitted to the hospital; however, it is not clear how acute intoxication affects recovery from a traumatic brain injury. Our group has previously shown that binge alcohol prior to traumatic brain injury resulted in long-term impairment in a fine sensorimotor task that was correlated with a decreased proliferative and neuroblast response from the subventricular zone. However, whether binge alcohol prior to traumatic brain injury affects the proliferative response in the hippocampal dentate gyrus is not yet known.

          Methods:

          Male rats underwent binge alcohol (3 g/kg/day) by gastric gavage for 3 days prior to traumatic brain injury. Cell proliferation was labeled by BrdU injections following traumatic brain injury. Stereological quantification and immunofluorescence confocal analysis of BrdU + cells in the hippocampal dorsal dentate gyrus was performed at 24 hours, 1 week and 6 weeks post traumatic brain injury.

          Results:

          We found that either traumatic brain injury alone or binge alcohol alone significantly increased dentate gyrus proliferation at 24 hours and 1 week. However, a combined binge alcohol and traumatic brain injury regimen resulted in decreased dentate gyrus proliferation at 24 hours post-traumatic brain injury. At the 6 week time point, binge alcohol overall reduced the number of BrdU + cells. Furthermore, more BrdU + cells were found in the dentate hilar region of alcohol traumatic brain injury compared to vehicle traumatic brain injury groups. The location and double-labeling of these mismigrated BrdU + cells was consistent with hilar ectopic granule cells.

          Conclusion:

          The results from this study showed that pre-traumatic brain injury binge alcohol impacts the injury-induced proliferative response in the dentate gyrus in the short-term and may affect the distribution of newly generated cells in the dentate gyrus in the long-term.

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          The epidemiology and impact of traumatic brain injury: a brief overview.

          Jean A Langlois, Wesley Rutland-Brown, Marlena M Wald (2006)
          Traumatic brain injury (TBI) is an important public health problem in the United States and worldwide. The estimated 5.3 million Americans living with TBI-related disability face numerous challenges in their efforts to return to a full and productive life. This article presents an overview of the epidemiology and impact of TBI.
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            Traumatic Brain Injury–Related Emergency Department Visits, Hospitalizations, and Deaths — United States, 2007 and 2013

            Christopher Taylor, Jeneita Bell, Matthew Breiding … (2017)
            Problem/Condition Traumatic brain injury (TBI) has short- and long-term adverse clinical outcomes, including death and disability. TBI can be caused by a number of principal mechanisms, including motor-vehicle crashes, falls, and assaults. This report describes the estimated incidence of TBI-related emergency department (ED) visits, hospitalizations, and deaths during 2013 and makes comparisons to similar estimates from 2007. Reporting Period 2007 and 2013. Description of System State-based administrative health care data were used to calculate estimates of TBI-related ED visits and hospitalizations by principal mechanism of injury, age group, sex, and injury intent. Categories of injury intent included unintentional (motor-vehicle crashes, falls, being struck by or against an object, mechanism unspecified), intentional (self-harm and assault/homicide), and undetermined intent. These health records come from the Healthcare Cost and Utilization Project’s National Emergency Department Sample and National Inpatient Sample. TBI-related death analyses used CDC multiple-cause-of-death public-use data files, which contain death certificate data from all 50 states and the District of Columbia. Results In 2013, a total of approximately 2.8 million TBI-related ED visits, hospitalizations, and deaths (TBI-EDHDs) occurred in the United States. This consisted of approximately 2.5 million TBI-related ED visits, approximately 282,000 TBI-related hospitalizations, and approximately 56,000 TBI-related deaths. TBIs were diagnosed in nearly 2.8 million (1.9%) of the approximately 149 million total injury- and noninjury-related EDHDs that occurred in the United States during 2013. Rates of TBI-EDHDs varied by age, with the highest rates observed among persons aged ≥75 years (2,232.2 per 100,000 population), 0–4 years (1,591.5), and 15–24 years (1,080.7). Overall, males had higher age-adjusted rates of TBI-EDHDs (959.0) compared with females (810.8) and the most common principal mechanisms of injury for all age groups included falls (413.2, age-adjusted), being struck by or against an object (142.1, age-adjusted), and motor-vehicle crashes (121.7, age-adjusted). The age-adjusted rate of ED visits was higher in 2013 (787.1) versus 2007 (534.4), with fall-related TBIs among persons aged ≥75 years accounting for 17.9% of the increase in the number of TBI-related ED visits. The number and rate of TBI-related hospitalizations also increased among persons aged ≥75 years (from 356.9 in 2007 to 454.4 in 2013), primarily because of falls. Whereas motor-vehicle crashes were the leading cause of TBI-related deaths in 2007 in both number and rate, in 2013, intentional self-harm was the leading cause in number and rate. The overall age-adjusted rate of TBI-related deaths for all ages decreased from 17.9 in 2007 to 17.0 in 2013; however, age-adjusted TBI-related death rates attributable to falls increased from 3.8 in 2007 to 4.5 in 2013, primarily among older adults. Although the age-adjusted rate of TBI-related deaths attributable to motor-vehicle crashes decreased from 5.0 in 2007 to 3.4 in 2013, the age-adjusted rate of TBI-related ED visits attributable to motor-vehicle crashes increased from 83.8 in 2007 to 99.5 in 2013. The age-adjusted rate of TBI-related hospitalizations attributable to motor-vehicle crashes decreased from 23.5 in 2007 to 18.8 in 2013. Interpretation Progress has been made to prevent motor-vehicle crashes, resulting in a decrease in the number of TBI-related hospitalizations and deaths from 2007 to 2013. However, during the same time, the number and rate of older adult fall-related TBIs have increased substantially. Although considerable public interest has focused on sports-related concussion in youth, the findings in this report suggest that TBIs attributable to older adult falls, many of which result in hospitalization and death, should receive public health attention. Public Health Actions The increase in the number of fall-related TBIs in older adults suggests an urgent need to enhance fall-prevention efforts in that population. Multiple effective interventions have been identified, and CDC has developed the STEADI initiative (Stopping Elderly Accidents Deaths and Injuries) as a comprehensive strategy that incorporates empirically supported clinical guidelines and scientifically tested interventions to help primary care providers address their patients’ fall risk through the identification of modifiable risk factors and implementation of effective interventions (e.g., exercise, medication management, and Vitamin D supplementation).
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              Doublecortin is a developmentally regulated, microtubule-associated protein expressed in migrating and differentiating neurons.

              F Francis, A Koulakoff, D. Boucher … (1999)
              Recently, we and others reported that the doublecortin gene is responsible for X-linked lissencephaly and subcortical laminar heterotopia. Here, we show that Doublecortin is expressed in the brain throughout the period of corticogenesis in migrating and differentiating neurons. Immunohistochemical studies show its localization in the soma and leading processes of tangentially migrating neurons, and a strong axonal labeling is observed in differentiating neurons. In cultured neurons, Doublecortin expression is highest in the distal parts of developing processes. We demonstrate by sedimentation and microscopy studies that Doublecortin is associated with microtubules (MTs) and postulate that it is a novel MAP. Our data suggest that the cortical dysgeneses associated with the loss of Doublecortin function might result from abnormal cytoskeletal dynamics in neuronal cell development.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neurosci Insights
                Journal ID (iso-abbrev): Neurosci Insights
                Journal ID (publisher-id): EXN
                Journal ID (hwp): spexn
                Title: Neuroscience Insights
                Publisher: SAGE Publications (Sage UK: London, England )
                ISSN (Electronic): 2633-1055
                Publication date (Electronic): 10 November 2020
                Publication date Collection: 2020
                Volume: 15
                Electronic Location Identifier: 2633105520968904
                Affiliations
                [1 ]Research Service, Edward Hines Jr. VA Hospital, Hines, IL, USA
                [2 ]Department of Molecular Pharmacology and Neuroscience, Loyola University Chicago Health Sciences Division, Maywood, IL, USA
                [3 ]Department of Mathematics and Statistics, and Institute of Environmental Sustainability, Loyola University Chicago, Chicago, IL, USA
                Author notes
                [*]Son T Ton, Research Service 151, Edward Hines Jr VA Hospital, 5000 S 5th Ave, Hines, IL 60141, USA. Email: son.ton@ 123456va.gov
                Author information
                https://orcid.org/0000-0002-4287-7412
                Article
                Publisher ID: 10.1177_2633105520968904
                DOI: 10.1177/2633105520968904
                PMC ID: 7672731
                SO-VID: e587b07c-a306-4ca0-a605-47e78500b575
                Copyright © © The Author(s) 2020
                License:

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Date received : 19 June 2020
                Date accepted : 6 October 2020
                Funding
                Funded by: u.s. department of veterans affairs, FundRef https://doi.org/10.13039/100000738;
                Funded by: NIH/NIAAA T32 AA01352, ;
                Funded by: the Kalmanovitz Center for CNS Repair, ;
                Funded by: NIH/NIAAA-R21 AA020951, ;
                Funded by: Office of Academic Affiliations VA Advanced Fellowship in Polytrauma/Traumatic Brain Injury Rehabilitation, ;
                Categories
                Subject: Original Research
                Custom metadata
                cover-date January-December 2020
                typesetter ts1

                Keywords: binge alcohol,traumatic brain injury,proliferation,hippocampal dentate gyrus,hilar ectopic granule cells
                Data availability:
                Keywords: binge alcohol, traumatic brain injury, proliferation, hippocampal dentate gyrus, hilar ectopic granule cells

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