Exercise induces age-dependent changes on epigenetic parameters in rat hippocampus: A preliminary study

Elsner, Viviane Rostirola; Lovatel, Gisele Agustini; Moysés, Felipe dos Santos; Bertoldi, Karine; Spindler, Christiano; Cechinel, Laura Reck; Muotri, Alysson R.; Siqueira, Ionara Rodrigues

doi:10.1016/j.exger.2012.11.011

Cited by 65 publications

(40 citation statements)

References 20 publications

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“…Such treatments may include pharmacological approaches that target relevant NPY or GABA A receptor subtypes or maneuvers that facilitate NPY or ALLO synthesis pharmacologically 105,124 or epigenetically, for example, via use of deacetylase inhibitors or exercise. [125][126][127] In fact, there is preliminary evidence for beneficial effects of exercise on PTSD symptoms, 128 as well as several psychological symptoms associated with PTSD and CP including anxiety, panic and depression, anger, hostility, perceived stress, and low self-esteem. 129 Exercise also has been a part of traditional cognitive-behavioral approaches to the management of CP.…”

Section: Therapeutic Strategiesmentioning

confidence: 97%

The Shared Neuroanatomy and Neurobiology of Comorbid Chronic Pain and PTSD

Scioli-Salter¹,

Forman

Otis

et al. 2015

The Clinical Journal of Pain

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Chronic pain and posttraumatic stress disorder (PTSD) are disabling conditions that affect biological, psychological, and social domains of functioning. Clinical research demonstrates that patients who are affected by chronic pain and PTSD in combination experience greater pain, affective distress, and disability than patients with either condition alone. Additional research is needed to delineate the interrelated pathophysiology of chronic pain and PTSD, with the goal of facilitating more effective therapies to treat both conditions more effectively; current treatment strategies for chronic pain associated with PTSD have limited efficacy and place a heavy burden on patients, who must visit various specialists to manage these conditions separately. This article focuses on neurobiological factors that may contribute to the coprevalence and synergistic interactions of chronic pain and PTSD. First, we outline how circuits that mediate emotional distress and physiological threat, including pain, converge. Secondly, we discuss specific neurobiological mediators and modulators of these circuits that may contribute to chronic pain and PTSD symptoms. For example, neuropeptide Y, and the neuroactive steroids allopregnanolone and pregnanolone (together termed ALLO) have antistress and antinociceptive properties. Reduced levels of neuropeptide Y and ALLO have been implicated in the pathophysiology of both chronic pain and PTSD. The potential contribution of opioid and cannabinoid system factors also will be discussed. Finally, we address potential novel methods to restore the normal function of these systems. Such novel perspectives regarding disease and disease management are vital to the pursuit of relief for the many individuals who struggle with these disabling conditions.

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Section: Therapeutic Strategiesmentioning

confidence: 97%

The Shared Neuroanatomy and Neurobiology of Comorbid Chronic Pain and PTSD

Scioli-Salter¹,

Forman

Otis

et al. 2015

The Clinical Journal of Pain

View full text Add to dashboard Cite

show abstract

“…In contrast, the expression pattern of DNMTs and HDAC were decreased in both regions following exercise [189]. Similarly, in another study, a single exercise session decreased both DNMT3b and DNMT1 levels in young adult rats [190]. The exercise protocol was shown to reduce H3-K9 methylation levels in young adult rats, whereas the single session reversed the changes in H3-K9 methylation levels induced by aging [190].…”

Section: Exercise-induced Epigenetic Alterations Relevant To Cvdmentioning

confidence: 84%

“…Similarly, in another study, a single exercise session decreased both DNMT3b and DNMT1 levels in young adult rats [190]. The exercise protocol was shown to reduce H3-K9 methylation levels in young adult rats, whereas the single session reversed the changes in H3-K9 methylation levels induced by aging [190]. Furthermore, a forced exercise protocol ameliorated aging-related memory decline, decreased pro-inflammatory markers and increased histone H4 acetylation levels in the hippocampus of 20-month-old rats [191].…”

Section: Exercise-induced Epigenetic Alterations Relevant To Cvdmentioning

confidence: 91%

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The relevance of epigenetics to occlusive cerebral and peripheral arterial disease

2015

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Athero-thrombosis of the arteries supplying the brain and lower limb are the main causes of stroke and limb loss. New therapies are needed to improve the outcomes of athero-thrombosis. Recent evidence suggests a role for epigenetic changes in the development and progression of ischaemic injury due to atherosclerotic occlusion of peripheral arteries. DNA hypermethylation have been associated with cardiovascular diseases. Histone post-translational modifications have also been implicated in atherosclerosis. Oxidized low-density lipoprotein regulated pro-inflammatory gene expression within endothelial cells is controlled by phosphorylation/acetylation of histone H3 and acetylation of histone H4 for example. There are a number of challenges in translating the growing evidence implicating epigenetics in atherosclerosis to improved therapies for patients. These include the small therapeutic window in conditions such as acute stroke and critical limb ischaemia, since interventions introduced in such patients need to act rapidly and be safe in elderly patients with many co-morbidities. Pre-clinical animal experiments have also reported conflicting effects of some novel epigenetic drugs, which suggest that further in-depth studies are required to better understand their efficacy in resolving ischaemic injury. Effective ways of dealing with these challenges are needed before epigenetic approaches to therapy can be introduced into practice.

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“…Se sabe, por ejemplo, que el BDNF es crucial para los procesos de señaliza-ción por calcio en neuronas glutamatérgicas que posteriormente exhiben fenómenos de plasticidad (Cechetti et al, 2008;Farmer et al, 2004;van Praag, 2008;van Praag, Kempermann & Gage, 1999;Zheng et al, 2006). También se ha demostrado que el uso de antagonistas de BDNF o la alteración en su expresión disminuyen la supervivencia neuronal y el aprendizaje (Abel & Rissman, 2013;Berchtold et al, 2010;Bertoldi et al, 2012;Elsner et al, 2011;Elsner et al, 2013;Gomez-Pinilla, Zhuang, Feng, Ying & Fan, 2011;Kaliman et al, 2011;Kong et al, 2010;Zajac et al, 2010). De acuerdo a lo anterior, es claro que muchas de las modificaciones estructurales y funcionales ocasionadas por actividad física estarían mediadas por interacciones tanto a nivel celular como posiblemente genético.…”

Section: Enriquecimiento Ambiental Ejercicio Y Actividad Físicaunclassified

Efectos del estrés sobre los procesos de plasticidad y neurogénesis: una revisión

Zarate¹,

Parra²,

Acevedo-Triana

et al. 2014

Univ Psychol

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r e S u M e n Grandes esfuerzos han sido llevados a cabo para entender los componentes psicobiológicos del estrés y de algunas de las psicopatologías relacionadas con él, tales como los trastornos de ansiedad (ansiedad generalizada o crisis de pánico) e incluso la depresión. Existen evidencias de que procesos como la neurogénesis y la plasticidad se ven enormemente afectados por muchos factores, entre ellos el estrés. En esta revisión se presentan algunos de los principales conceptos sobre la relación entre estrés, plasticidad y neurogé-nesis, a los que se ha llegado a partir de investigaciones realizadas -principalmente en modelos animales-, desde hace algunas décadas. Se realizará una diferenciación entre los efectos ocasionados por estrés crónico y agudo, tratando de establecer las interacciones que sobre estos efectos ejercen algunas variables tales como el género o el rango de edad, se enfatizarán los efectos comportamentales para finalmente revisar algunas de las formas de intervención actualmente más usadas para el tratamiento del estrés. Palabras clave estrés; plasticidad; neurogénesis a B S t r a C tThere is a growing interest in the comprehension of psychobiological mechanisms underlying stress and its relationships with many psychopathologies such as anxiety (i.e. generalized anxiety and panic attacks) or depression. There are several reports on the effects of stress on neurogenesis and plasticity. This review will discuss some of the core concepts on the relation between stress, plasticity and neurogenesis obtained during the last decades from research -mainly based in the use of animal models. The distinguishable effects between acute and chronic stress will also be discussed in relation to other factors as genre and age with an emphasis on behavioral effects. Some current therapeutic approaches will be reviewed as well.

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Exercise induces age-dependent changes on epigenetic parameters in rat hippocampus: A preliminary study

Cited by 65 publications

References 20 publications

The Shared Neuroanatomy and Neurobiology of Comorbid Chronic Pain and PTSD

The Shared Neuroanatomy and Neurobiology of Comorbid Chronic Pain and PTSD

The relevance of epigenetics to occlusive cerebral and peripheral arterial disease

Efectos del estrés sobre los procesos de plasticidad y neurogénesis: una revisión

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