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1
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Repeated co-treatment with imipramine and amantadine induces hippocampal brain-derived neurotrophic factor gene expression in rats

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Rogoz Z., Skuza G., Legutko B.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 2
The problem of drug-resistant depression indicates a strong need for alternative antidepressant therapies. In our earlier papers we described synergistic, antidepressant-like effects of a combination of imipramine (IMI) and amantadine (AMA) in the forced swimming test in rats, an animal model of depression. Moreover, preliminary clinical data showed that the above-mentioned combination had beneficial effects in treatment-resistant patients. In addition, a number of studies predicted a role of the brain-derived neurotrophic factor (BDNF) in the mechanism of action of antidepressant drugs (ADs). Since the most potent effect of ADs on BDNF gene expression was found after prolonged treatment, in the present study we investigated the influence of repeated treatment with IMI (5 or 10 mg/kg) and AMA (10 mg/kg), given separately or jointly (twice daily for 14 day), on mRNA level (the Northern blot) in the hippocampus and cerebral cortex. The experiment was carried out on male Wistar rats. The tissue for biochemical assays was dissected 24 h after the last dose of IMI and AMA. We also studied the effect of repeated treatment with IMI and AMA on the action of 5-HT1A- and 5-HT2A receptor agonists (8-OH-DPAT and (±)DOI, respectively) in behavioral tests. The obtained results showed that in the hippocampus IMI (10 mg/kg), and in the cerebral cortex IMI (5 and 10 mg/kg) and AMA (10 mg/kg) significantly elevated BDNF mRNA level. Joint administration of IMI (5 or 10 mg/kg) and AMA (10 mg/kg) induced a more potent increase BDNF gene expression in the hippocampus (but not in cerebral cortex) and either inhibited the behavioral syndrome induced by (±)DOI or did not change the action of 8-OH-DPAT (compared to treatment with either drug alone). The obtained results suggest that the enhancement of BDNF gene expression may be essential for the therapeutic effect of co-administration of IMI and AMA to drug-resistant depressed patients, and that among other mechanisms, 5-HT2A receptors possibly play some role in this effect.
2
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Repeated treatment with mirtazapine induces brain-derived neurotrophic factor gene expression in rats

100%
Rogoz Z., Skuza G., Legutko B.
Journal of Physiology and Pharmacology
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2005
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tom 56
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nr 4
Recent studies indicate a role of the brain-derived neurotrophic factor (BDNF) in the pathophysiology of depression, as well as in the mechanism of action of antidepressant drugs (ADs). It has been shown that serum BDNF levels are decreased in depressed patients. Moreover, antidepressant treatment increases serum BDNF levels and it is positively correlated with medication response. In addition, repeated administration of ADs induces an increase in rat hippocampal or cortical BDNF gene expression. Since the most potent effect of ADs on BDNF gene expression was found after prolonged treatment, in the present study we investigated the influence of repeated treatment (twice daily for 14 days) of the new AD mirtazapine (5 or 10 mg/kg) on BDNF mRNA level (the Northern blot) in rat hippocampus and cerebral cortex. Imipramine was used as a reference compound. The experiment was carried out on male Wistar rats. The tissue for biochemical assays was collected 24 h after the last doses of mirtazapine and imipramine. We also studied the effect of repeated mirtazapine on the action of the 5-HT2A receptor agonist (±)DOI in the behavioral test (head twitches induced by (±)DOI) in rats. The obtained results showed that, like imipramine (10 mg/kg), mirtazapine (10 mg/kg) increased BDNF gene expression in both the examined brain regions: in the hippocampus by 24.0 and 26.5%, in the cerebral cortex by 29.9 and 41.5%, respectively, compared with the vehicle-treated control. Neither mirtazapine nor imipramine administered repeatedly at a lower dose (5 mg/kg) significantly changed BDNF mRNA levels in the hippocampus and cerebral cortex. Repeated treatment with mirtazapine (10, but not 5 mg/kg) inhibited the behavioral syndrome induced by (±)DOI. This study provides first conclusive evidence that repeated mirtazapine administration increases BDNF mRNA levels; moreover, it indicates that the enhancement of BDNF gene expression may be essential for the clinical effect of mirtazapine.
3
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Effect of vitamin E on cerebral cortical oxidative stress and brain-derived neurotrophic factor gene expression induced by hypoxia and exercise in rats

84%
Sakr H. F., Abbasi A. M., El Samanoudy A. Z.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 2
4
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Crossfit training changes brain-derived neurotrophic factor and irisin levels at rest, after Wingate and progressive tests, and improves aerobic capacity and body composition of young physically active men and women

84%
Murawska-Cialowicz E., Wojna J., Zuwala-Jagiello J.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 6
5
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Maternal high-fat diet during pregnancy and lactation provokes depressive-like behavior and influences the irisin/brain-derived neurotrophic factor axis and inflammatory factors in male and female offspring in rats

84%
Gawlinska K., Gawlinski D., Przegalinski E., Filip M.
Journal of Physiology and Pharmacology
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2019
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tom 70
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nr 3
6
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Breast cancer surgery decreases serum brain-derived neurotrophic factor concentrations in middle aged women: relationship to the serum C-reactive protein concentration

84%
Zoladz J. A., Nowak L. R., Majerczak J., Kulpa J., Pilc A., Duda K.
Journal of Physiology and Pharmacology
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2019
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tom 70
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nr 4
7
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Moderate-intensity interval training increases serum brain-derived neurotrophic factor level and decreases inflammation in Parkinson's disease patients

84%
Zoladz J. A., Majerczak J., Zeligowska E., Mencel J., Jaskolski A., Marusiak J.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 3
8
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Endurance training increases plasma brain-derived neurotrophic factor concentration in young healthy men

67%
Zoladz J. A., Pilc A., Majerczak J., Grandys M., Zapart-Bukowska J., Duda K.
Journal of Physiology and Pharmacology. Supplement
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2008
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tom 59
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nr 7
9

Expression and localization of nerve growth factor (NGF) in the testis of alpaca (llama pacos)

67%
Wang H., Dong Y., Chen W., Hei J., Dong C.
Folia Histochemica et Cytobiologica
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2011
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tom 49
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nr 1
10
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Effects of sprint cycling and stretch-shortening cycle exercises on the neuromuscular, immune and stress indicators in young men

67%
Verbickas V., Baranauskiene N., Eimantas N., Kamandulis S., Rutkauskas S., Satkunskiene D., Sadauskas S., Brazaitis M., Skurvydas A.
Journal of Physiology and Pharmacology
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2017
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tom 68
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nr 1
11
Content available remote

Protective effects of vortioxetine in predator scent stress model of post-traumatic stress disorder in rats: role on neuroplasticity and apoptosis

67%
Ozbeyli D., Aykac A., Alaca N., Hazar-Yavuz A. N., Ozkan N., Sener G.
Journal of Physiology and Pharmacology
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2019
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tom 70
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nr 4
12

Brain-derived neurotrophic factor in neuroimmunology: lessons learned from multiple sclerosis patients and experimental autoimmune encephalomyelitis models

67%
Luhder F., Gold R., Flugel A., Linker R. A.
Archivum Immunologiae et Therapiae Experimentalis
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2013
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tom 61
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nr 2
13

Signalling pathways mediating anti-apoptotic action of neurotrophins

67%
Hetman M., Xia Z.
Acta Neurobiologiae Experimentalis
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2000
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tom 60
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nr 4
Neurotrophins promote survival and suppress apoptosis in many populations of neurons. Currently, phosphatidylinositol-3 kinase (PI-3K) is recognized as the main mediator of this protective effect. However, most of the data collected so far on the anti-apoptotic signaling of neurotrophins were obtained using trophic withdrawal paradigms. Recent data from our and other groups indicate that extracellular-signal-regulated kinase 1/2 (Erk1/2) may play a critical role in suppressing neuronal apoptosis triggered by cellular damage. Thus, it appears that either Erk1/2 or PI-3K, depending on the nature of the death-inducing stimulus, can mediate anti-apoptotic signaling of neurotrophins. In this review, we discuss the contribution of Erk1/2 and PI-3K to neuroprotection by neurotrophins. We also present data suggesting possible mechanisms by which these pathways might suppress neuronal death.
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