A behavioral analysis of the impact of voluntary physical activity on hippocampus‐dependent contextual conditioning

Greenwood, Benjamin N.; Strong, Paul V.; Foley, Teresa E.; Fleshner, Monika

doi:10.1002/hipo.20534

Cited by 86 publications

(100 citation statements)

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“…We performed the contextual fear conditioning test, which is one of the most useful tests assessing hippocampus-dependent memory. After exercise for three weeks, wild-type mice showed a significant enhancement of contextual freezing responses 24 hours after conditioning, as described previously [38] . Under no-exercise conditions, wild-type and htr3a-/-mice displayed a similar contextual fear learning ability, as described previously [10,11] .…”

Section: Reviewsupporting

confidence: 63%

Exercise-induced neuronal effects and the 5-HT3 receptor

Kondo

Shimada²

2015

Neurotransmitter

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Fourteen subtypes of the serotonin (5-hydroxytryptamine, 5-HT) receptor have been delineated, and these subtypes are assigned to seven 5-HT receptor subfamilies (5-HT1-7). Among the 5-HT receptor subfamilies, the 5-HT type 3 (5-HT3) receptor is the only ionotropic receptor. Previous studies have reported abundant expression of the 5-HT3 receptor in the hippocampus, and the involvement in the mood and memory. However, possible roles of the 5-HT3 receptor in hippocampal neurogenesis remains unknown. We performed immunohistochemical analyses of adult hippocampal neurogenesis in the 5-HT3A receptor-deficient mice (htr3a-/-mice). We found that basal cell proliferation and neurogenesis in the hippocampal dentate gyrus of htr3a-/-mice were normal. Exercise is known to increase hippocampal neurogenesis, cause antidepressant effects and enhance learning ability. Immunohistochemical and behavioral analyses of htr3a-/-mice revealed that a lack of the 5-HT3 receptor led to a blockade of the exercise-induced neurogenesis in the hippocampus and antidepressant effects, but not of enhanced learning ability. Moreover, we have shown that the 5-HT3 receptor agonist enhanced cell proliferation in the hippocampal dentate gyrus. Our results indicate that the 5-HT3 receptor is indispensable for increased hippocampal neurogenesis and antidepressant effects induced by exercise. Amongst the serotonin (5-hydroxytryptamine, 5-HT) receptor subfamilies [1] , the 5-HT3 receptor is the only ligand-gated ionotropic receptor [2,3] . Previous studies have shown that the 5-HT3 receptor is expressed in the limbic brain regions, such as hippocampus, amygdala and prefrontal cortex [4,5,6,] . Furthermore, many reports have indicated the involvement of the 5-HT3 receptor in emotional and cognitive functions, such as mood and memory [1,7,8,9,10,11] . The dentate gyrus of the hippocampus is a brain region where adult neurogenesis prominently occurs. As for the hippocampus, despite enriched expression of the 5-HT3 receptor, its possible roles in adult hippocampal neurogenesis remains uncertain. KeywordsIt is well known that exercise causes a variety of influences on brain structure and function [12,13] . The hippocampus is one of the brain regions affected by exercise stimulation. Actually, previous studies have shown that exercise induced increase in adult neurogenesis [14,15] and synaptogenesis [16,17] in the hippocampus at the morphological levels. The hippocampus is involved in the cognitive and emotional processes, and the altered function of the hippocampus has influences on animal behavior. Exercise has been reported to cause antidepressant effects [18,19,20,21,22] and learning enhancement [15,23,24] in human and rodents, and it is suggested that the hippocampus is implicated in these behavioral changes. Importantly, Neurotransmitter 2015; 2: e764. doi: 10.14800/nt. 764; © 2015 by Makoto Kondo, et al. http://www.smartscitech.com/index.php/nt Page 2 of 5 serotonin is thought to be one of the most important molecules that mediate these benefi...

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Section: Reviewsupporting

confidence: 63%

Exercise-induced neuronal effects and the 5-HT3 receptor

Kondo

Shimada²

2015

Neurotransmitter

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“…Despite the well-established benefits of chronic exercise on cognition and learning processes (Cotman and Berchtold 2002;Hillman et al 2003Hillman et al , 2014Cassilhas et al 2015;Prakash et al 2015), the lingering changes in the brain produced by habitual exercise are not sufficient to enhance fear extinction (Greenwood et al 2009). Moreover, maintenance of chronic exercise is essential for use in a clinical setting, yet maintaining regular exercise is a constant challenge and long-term exercise adherence rates are low (Dishman 1982;Hogg et al 2012;Zuckoff 2012) even when initial motivation is high (Van Roie et al 2015).…”

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confidence: 99%

Acute exercise enhances the consolidation of fear extinction memory and reduces conditioned fear relapse in a sex-dependent manner

et al. 2017

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Fear extinction-based exposure therapy is the most common behavioral therapy for anxiety and trauma-related disorders, but fear extinction memories are labile and fear tends to return even after successful extinction. The relapse of fear contributes to the poor long-term efficacy of exposure therapy. A single session of voluntary exercise can enhance the acquisition and consolidation of fear extinction in male rats, but the effects of exercise on relapse of fear after extinction are not well understood. Here, we characterized the effects of 2 h of voluntary exercise during the consolidation phase of contextual or auditory fear extinction learning on long-term fear extinction memory and renewal in adult, male and female, LongEvans rats. Results indicate that exercise enhances consolidation of fear extinction memory and reduces fear relapse after extinction in a sex-dependent manner. These data suggest that brief bouts of exercise could be used as an augmentation strategy for exposure therapy, even in previously sedentary subjects. Fear memories of discrete cues, rather than of contextual ones, may be most susceptible to exercise-augmented extinction, especially in males. Additionally, exercise seems to have the biggest impact on fear relapse phenomena, even if fear extinction memories themselves are only minimally enhanced.

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“…Physical exercise, for example, increases BDNF expression in the hippocampus, which is critically involved in memory processes 88,89 . Augmentation of the effects of exposure therapy with physical exercise has been tested in PTSD patients with promising results 90 .…”

Section: Discussionmentioning

confidence: 99%

Brain derived neurotrophic factor mediated learning, fear acquisition and extinction as targets for developing novel treatments for anxiety

Oliveira

Hounie

Cappi

et al. 2016

J. bras. psiquiatr.

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KeywordsBrain-derived neurotrophic factor, fear, anxiety disorders, learning, psychological extinction. Palavras-chaveFator neurotrófico derivado do cérebro, medo, transtornos de ansiedade, aprendizagem, extinção psicológica.Brain derived neurotrophic factor mediated learning, fear acquisition and extinction as targets for developing novel treatments for anxiety Aprendizado, aquisição ABSTRACTAnxiety and obsessive-compulsive related disorders are highly prevalent and disabling disorders for which there are still treatment gaps to be explored. Fear is a core symptom of these disorders and its learning is highly dependent on the activity of the neurotrophin brain--derived neurotrophic factor (BDNF). Should BDNF-mediated fear learning be considered a target for the development of novel treatments for anxiety and obsessive-compulsive related disorders? We review the evidence that suggests that BDNF expression is necessary for the acquisition of conditioned fear, as well as for the recall of its extinction. We describe the findings related to fear learning and genetic/epigenetic manipulation of Bdnf expression in animals and BDNF allelic variants in humans. Later, we discuss how manipulation of BDNF levels represents a promising potential treatment target that may increase the benefits of therapies that extinguish previously conditioned fear. RESUMOOs transtornos da ansiedade e o transtorno obsessivo-compulsivo (TOC) e transtornos relacionados são altamente prevalentes e incapacitantes. Apesar disso, ainda existem lacunas a serem exploradas em relação ao tratamento desses transtornos. O medo é um sintoma central desses transtornos e sua aprendizagem é altamente dependente da atividade do fator neurotrófico derivado do cérebro (BDNF). Porém, será que a aprendizagem de medo mediada pelo BDNF deve ser considerada um alvo para o desenvolvimento de novos tratamentos para transtornos da ansiedade, TOC e transtornos relacionados? Revisamos as evidências que sugerem que a expressão de BDNF é necessária para a aquisição do medo condicionado, bem como para a evocação de sua extinção. Descrevemos os resultados relacionados a aprendizagem de medo, manipulação genética e epigenética da expressão de Bdnf em animais e variantes alélicas de BDNF em seres humanos. Posteriormente, discutimos como a manipulação dos níveis de BDNF representa um alvo em potencial para o tratamento, o que pode aumentar os benefícios das terapias que extinguem o medo previamente condicionado. Oliveira KS et al.

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A behavioral analysis of the impact of voluntary physical activity on hippocampus‐dependent contextual conditioning

Cited by 86 publications

References 86 publications

Exercise-induced neuronal effects and the 5-HT3 receptor

Exercise-induced neuronal effects and the 5-HT3 receptor

Acute exercise enhances the consolidation of fear extinction memory and reduces conditioned fear relapse in a sex-dependent manner

Brain derived neurotrophic factor mediated learning, fear acquisition and extinction as targets for developing novel treatments for anxiety

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