Dizocilpine and cycloheximide prevent inhibition of c-Fos gene expression by delta sleep-inducing peptide in the paraventricular nucleus of the hypothalamus in rats with different resistance to emotional stress

Umriukhin, Pavel E.; Коплик, Е. В.; Судаков, К. В.

doi:10.1016/j.neulet.2011.11.001

Cited by 4 publications

(6 citation statements)

References 19 publications

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“…In other regions of the brain (the lateral septum and medial septum), the administration of DSIP led to a smaller decrease in c-Fos expression. Prevention of peptide-mediated inhibition of c-Fos expression upon administration of an NMDA receptor antagonist dizocilpine also supports the potential for DSIP to realize its effects via NMDA receptors [57].…”

Section: Discussionmentioning

confidence: 65%

DSIP-Like KND Peptide Reduces Brain Infarction in C57Bl/6 and Reduces Myocardial Infarction in SD Rats When Administered during Reperfusion

et al. 2021

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A structural analogue of the DSIP, peptide KND, previously showed higher detoxification efficacy upon administration of the cytotoxic drug cisplatin, compared to DSIP. DSIP and KND were investigated using the model of acute myocardial infarction in male SD rats and the model of acute focal stroke in C57Bl/6 mice. A significant decrease in the myocardial infarction area was registered in KND-treated animals relative to saline-treated control animals (19.1 ± 7.3% versus 42.1 ± 9.2%). The brain infarction volume was significantly lower in animals intranasally treated with KND compared to the control saline-treated animals (7.4 ± 3.5% versus 12.2 ± 5.6%). Injection of KND in the first minute of reperfusion in the models of myocardial infarction and cerebral stroke reduced infarction of these organs, indicating a pronounced cardioprotective and neuroprotective effect of KND and potentiality for the treatment of ischemia-reperfusion injuries after transient ischemic attacks on the heart and brain, when administered during the reperfusion period. A preliminary pilot study using the model of myocardial infarction with the administration of DSIP during occlusion, and the model of cerebral stroke with the administration of KND during occlusion, resulted in 100% mortality in animals. Thus, in the case of ischemia-reperfusion injuries of the myocardium and the brain, use of these peptides is only possible during reperfusion.

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Section: Discussionmentioning

confidence: 65%

DSIP-Like KND Peptide Reduces Brain Infarction in C57Bl/6 and Reduces Myocardial Infarction in SD Rats When Administered during Reperfusion

et al. 2021

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“…Thus, difference in intensity and duration of restraint seemed not to be the reason for the observed difference. To further confirm that the restraint produced a stress response in the restrained mice, we examined the global consequence of restraint stress in hypothalamus of neuroendocrine system [38]–[42], and found that restraint stress induced activation of oxytocin neurons in PVN and SON of hypothalamus as evidenced by induction of c-fos expression. It has been suggested that oxytocin may regulate stress-induced corticotropin-releasing hormone gene expression [38].…”

Section: Discussionmentioning

confidence: 99%

Behavioral Stress Fails to Accelerate the Onset and Progression of Plaque Pathology in the Brain of a Mouse Model of Alzheimer's Disease

Yuan

Chau

et al. 2013

PLoS ONE

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Conflicting findings exist regarding the link between environmental factors and development of Alzheimer's disease (AD) in a variety of transgenic mouse models of AD. In the present study, we investigated the effect of behavioral stress on the onset and progression of Aβ pathology in the brains of TgCRND8 mice, a transgenic mouse model of AD. One group of TgCRND8 mice was subjected to restraint stress starting at 1 month of age until they were 3 months old, while restraint stress in the second group started at 4 months of age until they were 6 months old. After 2 months of treatment, no differences in the soluble, formic acid extracted, or histologically detected Aβ deposition in the cortical and hippocampal levels were found between non-stressed and stressed mice. These results showed that restraint stress alone failed to aggravate amyloid pathology when initiated either before or after the age of amyloid plaque deposition in TgCRND8 mice, suggesting that if stress aggravated AD phenotype, it may not be via an amyloid-related mechanism in the TgCRND8 mice. These findings are indicative that plaque load per se may not be used as a significant criterion for evaluating the effect of stress on AD patients.

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“…У крыс с различной стрессоустойчивостью обнаруживаются значимые отличия в концентрации плазменного кортикостерона, электрической активности мозга, медиаторном обеспечении стресс-респонсивных центров [9]. К примеру, содержание моноаминов в гипоталамусе у высокоустойчивых животных выше, а содержание дофамина в стволовых структурах ниже, чем у низкоустойчивых [9]. В зависимости от стрессоустойчивости разнятся также паттерны активации нейронов стресс-реализующих систем.…”

Section: уровень экспрессии гена C-fos в мононуклеарных лейкоцитах ниunclassified

“…В паравентрикулярном ядре гипоталамуса после иммобилизации у высокоустойчивых животных наблюдается значительно больше Fos-позитивных клеток по сравнению с низкоустойчивой группой. Эти изменения, отражающие первый этап активации гипоталамо-гипофизарно-надпочечниковой оси, в свою очередь, связаны с разным содержанием моноаминов и глутамата в указанных структурах мозга [9]. Аналогичные паттерны активации -большее количество Fos-позитивных клеток в группе резистентных животных -имеют место также в лимбических структурах при стрессе [15].…”

Section: уровень экспрессии гена C-fos в мононуклеарных лейкоцитах ниunclassified

“…Хорошо известны физиологические отличия низко-и высокоустойчивых животных, к числу которых, например, относится разное медиаторное обеспечение стресс-респонсивных центров мозга [9]. Для исследований, посвященных ТЭС-терапии, эта разделение тем более важно, так как позволяет детализировать представления о гомеостатическом характере действия данного лечебного метода.…”

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Transcranial Electrotherapy Stimulation Modulates Stress-Induced C-Fos Expression in Peripheral Blood Mononuclear Cells in Rats With Different Resistance to Stress

Каде¹,

Polyakov²,

Agumava³

et al. 2018

СПНО (MPSE)

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TRANSCRANIAL ELECTROTHERAPY STIMULATION MODULATES STRESS-INDUCED C-FOS EXPRESSION IN PERIPHERAL BLOOD MONONUCLEAR CELLS IN RATS WITH DIFFERENT RESISTANCE TO STRESSis a recognized and unique peripheral biomarker of stress, stress-associated and psychiatric disorders. In our article, we studied the possibility of correction of transcranial electrotherapy stimulation (TES-therapy) of stress-induced c-fos expression in PBMC of rats with high or low resistance to stress, predicted from differences in their modified forced swim test results. As a model of combined stress, a modified forced swim test and orthostatic stress were used. The expression of the c-fos gene in PBMC was carried out by real-time polymerase chain reaction. Relative c-fos expression in low resistance control group (Me=0,03) was statistically significantly less than that in high resistance control group (Me=1,3). TES-therapy was accompanied by a statistically significant increase in relative c-fos expression (Me=1) in low resistance treatment group. In high resistance treatment group TES-therapy, on the contrary, was accompanied by a decrease in relative c-fos expression (Me=0,15). These effects reflect the systemic stress limiting action of TES-therapy, which has a pronounced homeostatic character.

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Dizocilpine and cycloheximide prevent inhibition of c-Fos gene expression by delta sleep-inducing peptide in the paraventricular nucleus of the hypothalamus in rats with different resistance to emotional stress

Cited by 4 publications

References 19 publications

DSIP-Like KND Peptide Reduces Brain Infarction in C57Bl/6 and Reduces Myocardial Infarction in SD Rats When Administered during Reperfusion

DSIP-Like KND Peptide Reduces Brain Infarction in C57Bl/6 and Reduces Myocardial Infarction in SD Rats When Administered during Reperfusion

Behavioral Stress Fails to Accelerate the Onset and Progression of Plaque Pathology in the Brain of a Mouse Model of Alzheimer's Disease

Transcranial Electrotherapy Stimulation Modulates Stress-Induced C-Fos Expression in Peripheral Blood Mononuclear Cells in Rats With Different Resistance to Stress

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