92 research outputs found
Differential Effects of Psychological and Physical Stress on the Sleep Pattern in Rats
In the present study, we investigated the acute effects of 2 different kinds of stress, namely physical stress (foot shock) and psychological stress (non-foot shock) induced by the communication box method, on the sleep patterns of rats. The sleep patterns were recorded for 6 h immediately after 1 h of stress. Physical and psychological stress had almost opposite effects on the sleep patterns: In the physical stress group, hourly total rapid eye movement (REM) sleep and total non-REM sleep were significantly inhibited, whereas psychological stress enhanced hourly total REM sleep but not total non-REM sleep. Further results showed that total REM sleep, total non-REM sleep, total sleep and the total number of REM sleep episodes in 5 h were reduced, and that sleep latency was prolonged compared to the control group. On the other hand, in the psychological stress group, the total REM sleep in 5 h was increased significantly due to the prolongation of the average duration of REM sleep episodes and reduced REM sleep latency. In addition, the plasma of corticosterone increased significantly after physical stress but not after psychological stress. These results suggested that the sleep patterns, particularly the patterns of REM sleep following physical and psychological stress, are probably regulated by 2 different pathways.</p
Inhibitory Effects of Valproate on Impairment of Y-maze Alternation Behavior Induced by Repeated Electroconvulsive Seizures and c-Fos Protein Levels in Rat Brains
We previously showed that inhibition of repeated electroconvulsive shock (ECS)-induced seizures through 7-day administration of anti-epileptic drugs suppressed the impairment of spontaneous alternation behavior in the Y-maze test in rats. To clarify the precise mechanism(s), we investigated the effect of valproate on such impairment and examined the levels of brain-derived neurotrophic factor (BDNF) and c-Fos protein in the prefrontal cortex and the hippocampus 24h after the last administration of ECS. Seven-day intraperitoneal (i.p.) administration of valproate (400mg/kg) suppressed the impairment of spontaneous alternation behavior. Repeated ECS increased the BDNF protein levels in the hippocampus and prefrontal cortex in the presence or absence of valproate, indicating that the increase in BDNF protein levels resulted from electrical stimulation. c-Fos protein levels were significantly decreased in the hippocampal dentate gyrus after repeated ECS, but valproate had no significant effect on decreased c-Fos protein levels. Valproate+ECS significantly increased the c-Fos protein levels of the prefrontal cortex compared with the ECS group. These findings suggest that the inhibitory effect of valproate on repeated ECS-induced impairment of spontaneous alternation behavior may be linked to the prefrontal cortex
Effects of Physical and Psychological Stress on 5-HT2A Receptor-mediated Wet-dog Shake Responses in Streptozotocin-induced Diabetic Rats.
Several epidemiological and clinical studies have indicated that the prevalence of psychiatric disorders is higher in diabetic patients than in the general population. In the present studies, we examined the behavioral changes in streptozotocin-induced diabetic rats, and investigated the effects of physical and psychological stress on the hippocampal BDNF levels and on the serotonin 2A (5-HT2A) receptor-mediated wet-dog shake responses. The streptozotocin (60 mg/kg, i.p.)-induced diabetes had no significant effects on the immobility time in the forced swim test or on locomotor activity in the open-field test. Moreover, there was no significant difference in the wet-dog shake responses induced by DOI, a 5-HT2A receptor agonist, between nondiabetic and diabetic rats. Five-day exposure to physical (electric footshock) and psychological (non-footshock) stress had no signifi cant effect on the hippocampal BDNF level in diabetic or nondiabetic rats. The 2 types of stress had no significant effect on the DOI-induced wet-dog shake responses in nondiabetic rats. In diabetic rats, the repeated exposure to physical stress markedly increased the DOI-induced wet-dog shake responses, but the repeated exposure to psychological stress had no effect. These results suggest that exposure to physical stress augmented the susceptibility to the wet-dog shake responses to 5-HT2A receptor stimulation in streptozotocin-induced diabetic rats
Berberine produces antidepressant-like effects in ovariectomized mice
Berberine has been reports to have antidepressant-like effects. However, it is seldom known whether berberine produces antidepressant-like effects in ovariectomized mice, which exhibit depressive-like responses. To examine the antidepressant-like effects of berberine in ovariectomized mice, behavioral tests were conducted, including the forced swimming test and the open field test. To elucidate the mechanisms, levels of BDNF, phosphorylated CREB and phosphorylated eEF2 were analyzed by western blotting, and c-Fos induction was examined by immunohistochemistry. In the forced swimming test, berberine decreased the immobility time in a dose-dependent manner, reversing the depressive-like effect observed in ovariectomized mice, and this effect was blocked by the 5-HT2 antagonist ketanserin. In addition, western blotting indicated that BDNF and peEF2 in the hippocampus, but not pCREB/CREB in the frontal cortex, were affected by berberine treatment. Furthermore, immunohistochemistry demonstrated that the reduction in c-Fos induced by ovariectomy were greater after berberine treatment. Ketanserin also antagonized the effect of berberine on the c-Fos expression. Our findings suggest that berberine exerts antidepressant-like effects in ovariectomized mice, and 5-HT2 receptor activation may be partially related to the antidepressant-like effects of the berberine by BDNF-CREB and eEF2 pathways
The Role of KLF4 in Alzheimer’s Disease
Krüppel-like factor 4 (KLF4), a member of the family of zinc-finger transcription factors, is widely expressed in range of tissues that play multiple functions. Emerging evidence suggest KLF4’s critical regulatory effect on the neurophysiological and neuropathological processes of Alzheimer’s disease (AD), indicating that KLF4 might be a potential therapeutic target of neurodegenerative diseases. In this review, we will summarize relevant studies and illuminate the regulatory role of KLF4 in the neuroinflammation, neuronal apoptosis, axon regeneration and iron accumulation to clarify KLF4’s status in the pathogenesis of AD
Stress in Regulation of GABA Amygdala System and Relevance to Neuropsychiatric Diseases
The amygdala is an almond-shaped nucleus located deep and medially within the temporal lobe and is thought to play a crucial role in the regulation of emotional processes. GABAergic neurotransmission inhibits the amygdala and prevents us from generating inappropriate emotional and behavioral responses. Stress may cause the reduction of the GABAergic interneuronal network and the development of neuropsychological diseases. In this review, we summarize the recent evidence investigating the possible mechanisms underlying GABAergic control of the amygdala and its interaction with acute and chronic stress. Taken together, this study may contribute to future progress in finding new approaches to reverse the attenuation of GABAergic neurotransmission induced by stress in the amygdala
The impact of PI3K inhibitors on breast cancer cell and its tumor microenvironment
The phosphoinositide 3-kinase (PI3K) pathway shows frequent aberrant alterations and pathological activation in breast cancer cells. While PI3K inhibitors have not achieved expectant therapeutic efficacy in clinical trials, and several studies provide promising combination strategies to substantially maximize therapeutic outcomes. Besides its direct impact on regulating cancer cells survival, PI3K inhibitors are also demonstrated to have an immunomodulatory impact based on the tumor microenvironment. Inhibition of the leukocyte-enriched PI3K isoforms may break immune tolerance and restore cytotoxic T cell activity by reprogramming the tumor microenvironment. In addition, PI3K inhibitors have pleiotropic effects on tumor angiogenesis and even induce tumor vascular normalization. In this review, we discuss the mechanism of PI3K inhibitor suppression of breast cancer cells and modulation of the tumor microenvironment in order to provide further thoughts for breast cancer treatment
Role of Leptin in Mood Disorder and Neurodegenerative Disease
The critical regulatory role of leptin in the neuroendocrine system has been widely reported. Significantly, leptin can improve learning and memory, affect hippocampal synaptic plasticity, exert neuroprotective efficacy and reduce the risk of several neuropsychiatric diseases. In terms of depression, leptin could modulate the levels of neurotransmitters, neurotrophic factors and reverse the dysfunction in the hypothalamic-pituitary-adrenal axis (HPA). At the same time, leptin affects neurological diseases during the regulation of metabolic homeostasis. With regards to neurodegenerative diseases, leptin can affect them via neuroprotection, mainly including Alzheimer’s disease and Parkinson’s disease. This review will summarize the mechanisms of leptin signaling within the neuroendocrine system with respect to these diseases and discuss the therapeutic potential of leptin
Effect of Inflammation on the Process of Stroke Rehabilitation and Poststroke Depression
A considerable body of evidence has shown that inflammation plays an important role in the process of stroke rehabilitation and development of poststroke depression (PSD). However, the specific molecular and cellular mechanisms involved remain unclear. In this review, we summarize how neuroinflammation affects stroke rehabilitation and PSD. We mainly focus on the immune/inflammatory response, involving astrocytes, microglia, monocyte-derived macrophages, cytokines (tumor necrosis factor alpha, interleukin 1), and microRNAs (microRNA-124, microRNA 133b). This review provides new insights into the effect of inflammation on the process of stroke rehabilitation and PSD and potentially offer new therapeutic targets of stroke and PSD
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