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      Treadmill exercise improves memory by up-regulating dopamine and down-regulating D 2 dopamine receptor in traumatic brain injury rats

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          Abstract

          Traumatic brain injury (TBI) causes a variety of neuropathological manifestations including cognitive, emotional, physiological and psychological deficits. Physical exercise is known to ameliorate neurological impairments induced by various brain injuries. We investigated the effects of treadmill exercise on memory impairments due to TBI in relation to dopamine and D 2 dopamine receptor. TBI was induced with an electromagnetic-controlled cortical impact device. The rats in the exercise groups were scheduled to run on a treadmill for 30 min once a day for 28 days after TBI induction. Then, step-down avoidance task, radial 8-arm maze test, immunohistochemistry for tyrosine hydroxylase (TH), and western blot for D 2 dopamine receptor were performed. TBI impaired short-term and spatial learning memories. TBI decreased TH expressions in the prefrontal cortex (PFC), striatum, hippocampus dentate gyrus, and substantia nigra (SN). By contrast, the expressions of D 2 dopamine receptor in the PFC, striatum, hippocampus, and SN were increased by TBI. Treadmill exercise alleviated the impairments of short-term and spatial learning memories observed in TBI rats. TH expression was decreased and D 2 dopamine receptor expression was increased in TBI rats. Treadmill exercise enhanced TH expression and suppressed D 2 dopamine receptor expression in TBI rats. TBI deteriorated short-term and spatial learning memories, in contrast, treadmill exercise alleviated the TBI-induced memory impairments by up-regulating dopamine level and down-regulating D 2 dopamine receptor expression.

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          Dopamine-dependent facilitation of LTP induction in hippocampal CA1 by exposure to spatial novelty.

          Michael Rowan, Roger Anwyl, William K Cullen … (2003)
          In addition to its role in memory formation, the hippocampus may act as a novelty detector. Here we investigated whether attention to novel events can promote the associative synaptic plasticity mechanisms believed to be necessary for storing those events in memory. We therefore examined whether exposure to a novel spatial environment promoted the induction of activity-dependent persistent increases in glutamatergic transmission (long-term potentiation, LTP) at CA1 synapses in the rat hippocampus. We found that brief exposure to a novel environment lowered the threshold for the induction of LTP. This facilitatory effect was present for a short period following novelty exposure but was absent in animals that explored a familiar environment. Furthermore, the facilitation was dependent on activation of D1/D5 receptors. These findings support an important role for dopamine-regulated synaptic plasticity in the storage of unpredicted information in the CA1 area.
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            Exercise-induced improvement in cognitive performance after traumatic brain injury in rats is dependent on BDNF activation.

            Grace Sophia Griesbach, David Allen Hovda, Fernando Gomez-Pinilla (2009)
            We have previously shown that voluntary exercise upregulates brain derived neurotrophic factor (BDNF) within the hippocampus and is associated with an enhancement of cognitive recovery after a lateral fluid percussion injury (FPI). In order to determine if BDNF is critical to this effect we used an immunoadhesin chimera (TrkB-IgG) that inactivates free BDNF. This BDNF inhibitor was administered to adult male rats two weeks after they had received a mild fluid percussion injury (FPI) or sham surgery. These animals were then housed with or without access to a running wheel (RW) from post-injury-day (PID) 14 to 20. On PID 21, rats were tested for spatial learning in a Morris Water Maze. Results showed that exercise counteracted the cognitive deficits associated with the injury. However this exercise-induced cognitive improvement was attenuated in the FPI-RW rats that were treated with TrkB-IgG. Molecules important for synaptic plasticity and learning were measured in a separate group of rats that were sacrificed immediately after exercise (PID 21). Western blot analyses showed that exercise increased the mature form of BDNF, synapsin I and cyclic-AMP response-element-binding protein (CREB) in the vehicle treated Sham-RW group. However, only the mature form of BDNF and CREB were increased in the vehicle treated FPI-RW group. Blocking BDNF (pre administration of TrkB-IgG) greatly reduced the molecular effects of exercise in that exercise-induced increases of BDNF, synapsin I and CREB were not observed. These studies provide evidence that BDNF has a major role in exercise's cognitive effects in traumatically injured brain.
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              Persistent cognitive dysfunction after traumatic brain injury: A dopamine hypothesis.

              James Bales, Amy Wagner, Anthony Kline … (2009)
              Traumatic brain injury (TBI) represents a significant cause of death and disability in industrialized countries. Of particular importance to patients the chronic effect that TBI has on cognitive function. Therapeutic strategies have been difficult to evaluate because of the complexity of injuries and variety of patient presentations within a TBI population. However, pharmacotherapies targeting dopamine (DA) have consistently shown benefits in attention, behavioral outcome, executive function, and memory. Still it remains unclear what aspect of TBI pathology is targeted by DA therapies and what time-course of treatment is most beneficial for patient outcomes. Fortunately, ongoing research in animal models has begun to elucidate the pathophysiology of DA alterations after TBI. The purpose of this review is to discuss clinical and experimental research examining DAergic therapies after TBI, which will in turn elucidate the importance of DA for cognitive function/dysfunction after TBI as well as highlight the areas that require further study.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Exerc Rehabil
                Journal ID (iso-abbrev): J Exerc Rehabil
                Title: Journal of Exercise Rehabilitation
                Publisher: Korean Society of Exercise Rehabilitation
                ISSN (Print): 2288-176X
                ISSN (Electronic): 2288-1778
                Publication date Collection: August 2019
                Publication date (Electronic): 28 August 2019
                Volume: 15
                Issue: 4
                Pages: 504-511
                Affiliations
                [1 ]Department of Physiology, College of Medicine, Kyung Hee University, Seoul, Korea
                [2 ]Department of Oriental Sports Medicine, College of Biomedical Science, Daegu Haany University, Gyeongsan, Korea
                Author notes
                [* ]Corresponding author: Hong Kim, https://orcid.org/0000-0001-8740-3600, Department of Oriental Sports Medicine, College of Biomedical Science, Daegu Haany University, 1 Haanydae-ro, Gyeongsan 38610, Korea, E-mail: joshua@ 123456dhu.ac.kr
                Author information
                http://orcid.org/0000-0001-8740-3600
                Article
                Publisher ID: jer-15-4-504
                DOI: 10.12965/jer.1938316.158
                PMC ID: 6732546
                SO-VID: a94f9f8f-b60b-4c43-9d89-c360432274da
                Copyright © Copyright © 2019 Korean Society of Exercise Rehabilitation
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 7 May 2019
                Date accepted : 16 June 2019
                Categories
                Subject: Original Article

                Keywords: brain injuries,exercise,memory,dopamine,dopamine d2 receptor
                Data availability:
                Keywords: brain injuries, exercise, memory, dopamine, dopamine d2 receptor

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