Evidence of lasting dysregulation of neuroendocrine and HPA axis function following global cerebral ischemia in male rats and the effect of Antalarmin on plasma corticosterone level

Tremblaye, Patricia B. de la; Raymond, Julie; Milot, Marc R.; Merali, Zul; Plamondon, Hélène

doi:10.1016/j.yhbeh.2014.01.003

Cited by 35 publications

(23 citation statements)

References 80 publications

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“…The current findings are in agreement with previous reports of altered CORT following global ischemia (De la Tremblaye et al, 2014) and extend these observations to the more mild condition of microvascular ischemia. In the case of global ischemia, increased CORT levels are detected for a short period of time following injury before returning to baseline.…”

Section: Discussionsupporting

confidence: 93%

“…In the case of global ischemia, increased CORT levels are detected for a short period of time following injury before returning to baseline. Thereafter, and for up to 1 month, CORT responses to subsequent stressors are enhanced (De la Tremblaye et al, 2014). These findings are replicated in the current set of experiments despite the comparatively mild physiological effects of ME and the young age of the rats used in the current experiment (Merrett et al, 2010).…”

Section: Discussionsupporting

confidence: 71%

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Microemboli alter the acute stress response and cause prolonged expression of MCP-1 in the hippocampus

Nemeth

Neigh

2015

Psychoneuroendocrinology

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 71%

Microemboli alter the acute stress response and cause prolonged expression of MCP-1 in the hippocampus

Nemeth

Neigh

2015

Psychoneuroendocrinology

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“…Similar to what is observed following SE, the magnitude of HPA axis hyperactivity following stroke correlates with poor post-stroke prognosis [62]. In animal models, recent evidence suggests that HPA axis dysfunction following global cerebral ischemia may be long lasting [63]. This study demonstrated that although baseline corticosterone levels were normal seven days post-injury, stress-induced hyper-secretion of corticosterone was present 27 days post-injury.…”

Section: Hpa Axis Dysfunction In Tlesupporting

confidence: 72%

Hypothalamic-pituitary-adrenocortical axis dysfunction in epilepsy

Wulsin

Solomon

Privitera

et al. 2016

Physiology & Behavior

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“…Increased stress has even been suggested to exacerbate neuronal cell death by increasing neuroinflammation, which in turn is neurotoxic (de Pablos et al., 2014). Indeed, several studies have shown that stress increase the vulnerability to inflammation resulting in increased microglial activation and neuronal damage in different brain regions such as hippocampus (Espinosa-Oliva et al., 2011), substantia nigra (de Pablos et al., 2014) and prefrontal cortex (de Pablos et al., 2006). Furthermore, the same studies also showed that these effects of stress were dependent on glucocorticoid receptor signaling.…”

Section: Discussionmentioning

confidence: 99%

Forced treadmill exercise can induce stress and increase neuronal damage in a mouse model of global cerebral ischemia

Svensson

Rosvall

Boza-Serrano

et al. 2016

Neurobiology of Stress

116

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Physical exercise is known to be a beneficial factor by increasing the cellular stress tolerance. In ischemic stroke, physical exercise is suggested to both limit the brain injury and facilitate behavioral recovery. In this study we investigated the effect of physical exercise on brain damage following global cerebral ischemia in mice. We aimed to study the effects of 4.5 weeks of forced treadmill running prior to ischemia on neuronal damage, neuroinflammation and its effect on general stress by measuring corticosterone in feces. We subjected C57bl/6 mice (n = 63) to either treadmill running or a sedentary program prior to induction of global ischemia. Anxious, depressive, and cognitive behaviors were analyzed. Stress levels were analyzed using a corticosterone ELISA. Inflammatory and neurological outcomes were analyzed using immunohistochemistry, multiplex electrochemoluminescence ELISA and Western blot. To our surprise, we found that forced treadmill running induced a stress response, with increased anxiety in the Open Field test and increased levels of corticosterone. In accordance, mice subjected to forced exercise prior to ischemia developed larger neuronal damage in the hippocampus and showed higher cytokine levels in the brain and blood compared to non-exercised mice. The extent of neuronal damage correlated with increased corticosterone levels. To compare forced treadmill with voluntary wheel running, we used a different set of mice that exercised freely on running wheels. These mice did not show any anxiety or increased corticosterone levels. Altogether, our results indicate that exercise pre-conditioning may not be beneficial if the animals are forced to run as it can induce a detrimental stress response.

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Evidence of lasting dysregulation of neuroendocrine and HPA axis function following global cerebral ischemia in male rats and the effect of Antalarmin on plasma corticosterone level

Cited by 35 publications

References 80 publications

Microemboli alter the acute stress response and cause prolonged expression of MCP-1 in the hippocampus

Microemboli alter the acute stress response and cause prolonged expression of MCP-1 in the hippocampus

Hypothalamic-pituitary-adrenocortical axis dysfunction in epilepsy

Forced treadmill exercise can induce stress and increase neuronal damage in a mouse model of global cerebral ischemia

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