Cell proliferation in the hippocampus and in the heart is modified by exposure to repeated stress and treatment with memantine

Babic, S.; Ondrejcakova, Maria; Bakoš, Ján; Račeková, Enikő; Ježová, Daniela

doi:10.1016/j.jpsychires.2012.01.002

Cited by 14 publications

(12 citation statements)

References 46 publications

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“…A recognized negative consequence of chronic stress is impairment of brain plasticity (Mirescu & Gould 2006, Babic et al 2012 and this was also demonstrated in the present experiments. A significant decrease in cell proliferation, reflected by lower levels of BrdU incorporated into the DNA, was observed.…”

Section: Discussionsupporting

confidence: 85%

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Effects of atosiban on stress-related neuroendocrine factors

Babic¹,

Pokusa²,

Danevova³

et al. 2015

Journal of Endocrinology

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Atosiban, an oxytocin/vasopressin receptor antagonist, is used to decrease preterm uterine activity. The risk of preterm delivery is undoubtedly associated with stress, but potential side effects of atosiban on neuroendocrine functions and stress-related pathways are mostly unknown. These studies were designed to test the hypothesis that the chronic treatment of rats with atosiban modulates neuroendocrine functions under stress conditions. Male rats were treated (osmotic minipumps) with atosiban (600 mg/kg per day) or vehicle and were restrained for 120 min/day for 14 days. All animals were treated with a marker of cell proliferation 5-bromo-2-deoxyuridine. Anxiety-like behavior was measured using an elevated plus-maze. Treatment with atosiban failed to modify plasma concentrations of the stress hormones ACTH and corticosterone, but led to a rise in circulating copeptin. Atosiban increased prolactin levels in the non-stressed group. Oxytocin receptor mRNA levels were increased in rats exposed to stress. Treatment with atosiban, in both control and stressed animals, resulted in a decrease in oxytocin receptor gene expression in the hypothalamus. No changes were observed in vasopressin receptor 1A and 1B gene expression. The decrease in hippocampal cell proliferation induced by stress exposure was not modified by atosiban treatment. This study provides the first data, to our knowledge, revealing the effect of atosiban on gene expression of oxytocin receptors in the brain. Atosiban-induced enhancement of plasma copeptin indicates an elevation in vasopressinergic tone with potential influence on water-electrolyte balance.

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Section: Discussionsupporting

confidence: 85%

“…DNA concentrations were measured photometrically (GeneQuant Pro, Biochrom Ltd, Cambridge, UK) at a wavelength of 260 nm and stored at 4-7 8C. BrdU incorporation into DNA was measured by ELISA as described previously (Babic et al 2012, Babic & Jezova 2014.…”

Section: Analysis Of Cell Proliferation In the Hippocampusmentioning

confidence: 99%

Effects of atosiban on stress-related neuroendocrine factors

Babic¹,

Pokusa²,

Danevova³

et al. 2015

Journal of Endocrinology

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“…On the other hand, it has been found that memantine injection prevents stress-induced cell production decline in the hippocampus. In this regard, restraint stress applied for 2 h/day for seven days reduces cell proliferation in hippocampus which was inhibited by memantine [24]. …”

Section: Introductionmentioning

confidence: 99%

Inhibitory Effect of NMDA Receptors in the Ventral Tegmental Area on Hormonal and Eating Behavior Responses to Stress in Rats

Nasihatkon

Khosravi

Bourbour

et al. 2014

Behavioural Neurology

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Background. Stress and its consequences are among the causes of accidents. Objective. The effects of intraventral tegmental area (I-VTA) memantine on the plasma corticosterone and eating parameters disturbance induced by acute stress were investigated. Methods. Male Wistar rats (W: 250–300 g) were divided into control and experiential groups, each of which received memantine either intra-VTA or peripherally. One week after bilateral cannulation, the rats received memantine (1 and 5 μg/Rat) five min before electroshock stress. The other experimental groups received memantine (1 and 5 mg/kg) intraperitoneally 30 min before stress. The control groups received saline or memantine but did not experience stress. Food and water intake and plasma corticosterone level were recorded. Results. Results showed that stress decreases food intake but does not change water intake and increase in plasma corticosterone level. Intraperitoneal memantine administration slightly inhibits the stress effects on food intake. However, water intake and plasma corticosterone level were increased. Intra-VTA memantine reduces the effects of stress on corticosterone and water intake. Conclusion. It could be concluded that inhibition of glutamate NMDA receptors in the VTA by memantine leads to the inhibition of the eating behavior parameters and plasma corticosterone level disturbance induced by stress in rats.

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“…Primary monoclonal anti-BrdU antibody (formalin grade; Roche) was purified on hightrap affinity columns (1 ml rProtein A FF, Amersham Biosciences, Uppsala, Sweden). The BrdU ELISA was performed as described previously [21]. Shortly, the plates were coated with a solution of the anti-BrdU.…”

Section: Analysis Of Brdu Incorporation Into the Dnamentioning

confidence: 99%

“…Moreover, forced treadmill exercise leads to enhanced cell proliferation in the heart as measured via 5-bromo-2′-deoxyuridine (BrdU) incorporation into the newly formed DNA [18][19][20]. We have found previously an opposite effect, namely a pronounced reduction of the new cells formed in the heart induced by chronic stress exposure [21]. To our knowledge, no information is available on cell proliferation in the heart following voluntary exercise.…”

Section: Introductionmentioning

confidence: 99%

Opposite Effects of Voluntary Physical Exercise on β3-Adrenergic Receptors in the White and Brown Adipose Tissue

et al. 2019

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Catecholamine effects via β3-adrenergic receptors are important for the metabolism of the adipose tissue. Physical exercise is a core component of antiobesity regimens. We have tested the hypothesis that voluntary wheel running results in enhancement of β3-adrenergic receptor gene expression in the white and brown adipose tissues. The secondary hypothesis is that dietary tryptophan depletion modifies metabolic effects of exercise. Male Sprague-Dawley rats were assigned for sedentary and exercise groups with free access to running wheels for 3 weeks. All animals received normal control diet for 7 days. Both groups were fed either by low tryptophan (0.04%) diet or by control diet (0.2%) for next 2 weeks. The β3-adrenergic receptor mRNA levels in response to running increased in the retroperitoneal and epididymal fat pads. The gene expression of uncoupling protein-1 (UCP-1) was increased in the brown, while unchanged in the white fat tissues. Unlike control animals, the rats fed by low tryptophan diet did not exhibit a reduction of the white adipose tissue mass. Tryptophan depletion resulted in enhanced concentrations of plasma aldosterone and corticosterone, but had no influence on exercise-induced adrenal hypertrophy. No changes in β3-adrenergic receptor and cell proliferation measured by 5-bromo-2′-deoxyuridine incorporation in left heart ventricle were observed. The reduced β3-adrenergic receptor but not enhanced uncoupling protein-1 gene expression supports the hypothesis on hypoactive brown adipose tissue during exercise. Reduction in dietary tryptophan had no major influence on the exercise-induced changes in the metabolic parameters measured.

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Cell proliferation in the hippocampus and in the heart is modified by exposure to repeated stress and treatment with memantine

Cited by 14 publications

References 46 publications

Effects of atosiban on stress-related neuroendocrine factors

Effects of atosiban on stress-related neuroendocrine factors

Inhibitory Effect of NMDA Receptors in the Ventral Tegmental Area on Hormonal and Eating Behavior Responses to Stress in Rats

Opposite Effects of Voluntary Physical Exercise on β3-Adrenergic Receptors in the White and Brown Adipose Tissue

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