Project description:Vagus nerve stimulation (VNS) has been shown to enhance learning and memory, yet the mechanisms behind these enhancements are unknown. We show that VNS altered the hippocampal, cortical, and blood epigenetic transcriptomes in male Sprague Dawley rats whether or not the rats performed a novelty preference behavioral task. In the hippocampus, novelty preference correlated with decreased histone deacetylase 11 (HDAC11), a transcriptional repressor enriched in CA1 cells important for memory consolidation. In the cortex, the immediate early gene (IEG) ARC was increased in VNS rats and correlated with transcription of plasticity genes and epigenetic regulators, including HDAC3. For rats performing the novelty preference task, ARC correlated with performance. Surprisingly, VNS did not significantly reduce transcription of cortical or hippocampal proinflammatory cytokines. However, TNFRSF11B (osteoprotegerin) correlated with novelty preference as well as plasticity, stress–response signaling, and epigenetic regulation in both hippocampus and cortex. Together, our findings provide the first evidence that VNS induces widespread changes in the cognitive epigenetic landscape and specifically affects epigenetic modulators associated with novelty preference, stress–response signaling, memory consolidation, and cortical neural remodeling.
Project description:This study investigated the effect of Vagus Nerve Stimulation (VNS) on innate neuroinflammation and remyelination in lysolecithin (LPC) induced demyelination, a preclinical model for Multiple Sclerosis (MS). In a first experiment (demyelination experiment), LPC was injected in the corpus callosum of 33 Lewis rats, inducing a demyelinated lesion, and rats were treated with either continuously-cycled VNS (cVNS) or one-minute per day VNS (1minVNS) or sham VNS, from two days before the injection until three days post-injection (dpi), when they were killed for immunohistochemistry and proteomics analysis. This timepoint corresponded with a demyelinated lesion and peak inflammation. In a second experiment (remyelination experiment), 13 rats were analogously treated with either cVNS or sham from two days before LPC injection until 11 dpi, when they were killed for tissue prelevation for immunohistochemistry and proteomics. This timepoints corresponded with partial remyelination of the lesion. For proteomics analysis, 20 rats were randomly selected, namely five cVNS and five sham rats of the demyelination experiment, and five cVNS and five sham rats of the remyelination experiment.
Project description:Our previous findings suggest that the nucleus of the solitary tract (NTS), a pivotal region for regulating the set-point of arterial pressure, exhibits abnormal inflammation in pre-hypertensive and spontaneously hypertensive rats (SHRs) together with elevated anti-apoptotic and low apoptotic factor levels compared with that of normotensive Wistar–Kyoto (WKY) rats. Whether this chronic condition affects neuronal growth and plasticity in the NTS remains unknown. To unveil the characteristics of the neurodevelopmental environment in the NTS of hypertensive rats, we investigated the gene expression profile of neurotrophins and their receptors in SHRs compared to that of normotensive rat WKY.
Project description:Effects of voluntary exercise in rat aorta. Spontaneously hypertensive rats (SHR) performed 5 weeks of voluntary exercise (wheel-cage running). Aortic tissue was collected and samples were pooled (3 aortae/chip). Aortae from running rats were compared to aortae from non-running rats. Keywords: parallel sample
Project description:Time-course gene expression profiles were obtained from lung tissues of the rats treated with room air, intermittent- (IH) or sustained hypoxia (SH) for 1, 3, 7, 14 and 30 days using CodeLink microarrays. Using a systems biology approach, we observed that two different mechanisms are involved in the lung responses to IH and SH: IH leads to increased G-protein coupled signaling-, ion transport-, neuronal- and steroid hormone receptor activities; whereas SH causes increased blood vessel morphogenesis and immune responses. Our results provide insight into molecular mechanisms underlying IH and SH. Keywords: gene expression array-based, count rats were treated with intermittent- (IH) or sustained hypoxia (SH) for 1, 3, 7, 14 and 30 days; rats treated with room air were used as controls; gene expression profiles were obtained from these rats
Project description:Transcription profiling of rat left ventricular samples from 12-, 16- and 20-month old spontaneously hypertensive rats (SHRs) compared with age-matched Wistar-Kyoto (WKY) rats as controls
Project description:Transcription profiling of spontaneously hypertensive heart failure rats (SHHF) and a reference strain to identify heart failure susceptibility genes