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Background To understand brain function in health and disease, functional magnetic resonance imaging (fMRI) is widely used in rodent models. Because animals need to be immobilised for image acquisition, fMRI is commonly performed under anaesthesia. The choice of anaesthetic protocols and may affect fMRI readouts, either directly or via changing physiological balance, and thereby threaten the scientific validity of fMRI in rodents. Methods The present study systematically reviewed the literature investigating the influence of different anaesthesia regimes and changes in physiological parameters as confounders of blood oxygen level dependent (BOLD) fMRI in rats and mice. Four databases were searched, studies selected according to pre-defined criteria, and risk of bias assessed for each study. Results are reported in two separate articles; this part of the review focuses on effects of changes in physiological parameters. Results A total of 121 publications was included, of which 49 addressed effects of changes in physiological parameters. Risk of bias was high in all included studies. Blood oxygenation [arterial partial pressure of oxygen (paO2)], ventilation [arterial partial pressure of carbon dioxide (paCO2)] and arterial blood pressure affected BOLD fMRI readouts across various experimental paradigms. Conclusions Blood oxygenation, ventilation and arterial blood pressure should be monitored and maintained at stable physiological levels throughout experiments. Appropriate anaesthetic management and monitoring are crucial to obtain scientifically valid, reproducible results from fMRI studies in rodent models.Intracerebral hemorrhage (ICH) is a major type of cerebrovascular disease with poor prognosis. Recent studies have shown that Glycyl-l-histidyl-l-lysine (GHK) is a kind of natural human tripeptide which could inhibit inflammation and against neurodegenerative diseases, but neither its role nor the mechanisms in ICH have yet been explicit. Currently, we investigated the possible strategies of GHK on ICH injury. Neurological deficit scores, brain water content, Nissl staining, and aquaporin 4 (AQP4) immunohistochemistry were detected in different groups of rats. The expression of microRNAs (miRNAs) was examined by real-time PCR. Inflammatory factors were detected using enzyme-linked immunosorbent assay (ELISA). Cell viability and cell proliferation were detected by Cell Counting Kit-8 (CCK-8). Matrix metalloproteinase 2 (MMP2), MMP9, tissue inhibitors of metalloproteinase-1 (TIMP1), AQP4 expression were detected/assessed using western blot. We observed that 5 and 10 μg/g of GHK improved neurological recovery by significantly reducing brain water content, improving neurological deficits, and promoting neuron survival. this website Besides, GHK alleviated inflammatory reaction and downregulated AQP4 expression. Furthermore, the effects of GHK on astrocyte were associated with the upregulation of miRNA-146a-3p, which partially regulated the expression of AQP4. Our results demonstrated that the phosphatidylinositol 3-kinase (PI3K)/AKT pathway participated in the GHK-induced upregulation of miR-146a-3p and miR-146a-3p/AQP4 interaction plays a role in the injury following ICH. These findings suggested that GHK could provide a novel therapeutic strategy for ICH.Schizophrenic patients often do not have the sense that they direct their own movements or author their own thoughts (passivity phenomena). As willing must precede movement to be causal and thus generate the sense of agency, it is possible that the timing between the senses of willing and movement is shortened in schizophrenia. We tested the subjective perception of this time interval in patients with schizophrenia using a method based on Libet's paradigm, in which subjects specify a time W - the time of willing a movement - and a time M - the time that movement occurred. Patients with schizophrenia and healthy volunteers made voluntary movements at times of their own choice while looking at a fast-rotating clock on a computer screen and reported when their movements were willed and made. We recorded surface electromyography to determine the time of actual movement, and electroencephalography to record brain potentials associated with movement. Results showed a significantly reduced interval between the reported M and W in patients with respect to the healthy volunteers (p 0.05), while the control group experienced a time W at 100 ms prior to movement onset and this differed significantly from their time M at 19 ms prior to movement onset (p less then 0.01). These results suggest that patients with schizophrenia do have an altered timing of awareness of action - or an impaired judgment of the sequence of events - and that this might be etiologic in the development of the abnormal sense of agency.Prenatal stress (PS) can lead to neuroendocrine and emotional disorders later in adolescence. Sexual dimorphism in these neurodevelopmental outcomes have been observed; however, the underlying mechanisms are not fully understood. To address this issue, we investigated whether there are sex differences in epigenetic reprogramming in rats exposed to PS. Pregnant female rats were subjected to chronic restraint stress from gestational day (G)12 to G18. From postnatal day (P)38 to P45, subgroups of offspring including both males and females were subjected to behavioral testing and brain tissue specimens were analyzed by DNA pyrosequencing, western blotting, and Golgi staining to assess changes in methylation pattern of glucocorticoid receptor (GR) gene, expression of DNA methyltransferase (DNMT) and DNA demethylase, and dendrite morphology, respectively. The DNA methyltransferase inhibitor decitabine was administered to rats prior to PS to further evaluate the role of methylation in the sexually dimorphic effects of PS. The results showed that PS increased anxiety-like behavior in offspring, especially in females, while depression-like behavior was increased in male offspring compared to control littermates. The methylation pattern in the promoter region of the GR gene differed between males and females. Sex-specific changes in the expression of DNMTs (DNMT1 and DNMT3a) and DNA demethylase (Tet methylcytosine dioxygenase 2) were also observed. Interestingly, decitabine alleviated the behavioral disorder caused by PS and restored dendrite density and morphology in female but not male rats. These findings suggest that different change patterns of DNMT and demethylase in the two sexes after PS are responsible for the sexually dimorphism, which could have implications for the clinical management of stress-related disorders.
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