Neuroplasticity pathways and protein-interaction networks are modulated by vortioxetine in rodents

Additional file 2: Figure S1. Merged mouse and rat network (mapped to human proteins) and summary of biological functions of each sub-network. Biological functions were manually extracted from the Function and Gene Ontology fields of the UniProt protein entries. The genes with dark, bold borders were used to build the network of protein–protein interaction partners. Squares with bold borders represent upregulated targets from the rat network, and circles with bold borders indicate differentially-regulated targets from the mouse network. The arrowheads indicate the common targets found in mouse and rat networks. This network of physically-interacting proteins containing clusters related to synaptic plasticity, synaptic transmission, neurodevelopment, cell growth, metabolism, and apoptosis, was significantly modulated in both mouse and rat

Increased stress-evoked nitric oxide signalling in the Flinders sensitive line (FSL) rat: a genetic animal model of depression

Stress engenders the precipitation and progression of affective disorders, while stress-related release of excitatory mediators is implicated in the degenerative pathology observed especially in the hippocampus of patients with severe depression. Nitric oxide (NO) release following stress-evoke

Dietary magnesium deficiency alters gut microbiota and leads to depressive-like behaviour

Objective: Gut microbiota (GM) has previously been associated with alterations in rodent behaviour, and since the GM is affected by the diet, the composition of the diet may be an important factor contributing to behavioural changes. Interestingly, a magnesium restricted diet has been shown to induce anxiety and depressive-like behaviour in humans and rodents, and it could be suggested that magnesium deficiency may mediate the effects through an altered GM. Methods: The present study therefore fed C57BL/6 mice with a standard diet or a magnesium deficient diet (MgD) for 6 weeks, followed by behavioural testing in the forced swim test (FST) to evaluate depressive-like behaviour. An intraperitoneal glucose tolerance test (GTT) was performed 2 day after the FST to assess metabolic alterations. Neuroinflammatory markers were analysed from hippocampus. GM composition was analysed and correlated to the behaviour and hippocampal markers. Results: It was found that mice exposed to MgD for 6 weeks were more immobile than control mice in the FST, suggesting an increased depressive-like behaviour. No significant difference was detected in the GTT. GM composition correlated positively with the behaviour of undisturbed C57BL/6 mice, feeding MgD diet altered the microbial composition. The altered GM correlated positively to the hippocampal interleukin-6. Conclusion: In conclusion, we hypothesise that imbalances of the microbiota–gut–brain axis induced by consuming a MgD diet, contributes to the development of depressive-like behaviou

Intramuscular BoNT/A injections cause an inflammatory response in the muscle tissue of rats

Objectives The purpose of the present study was to investigate whether intramuscular BoNT/A injections cause an systemic inflammatory response and a local inflammatory response in the muscle tissue. Methods Thirty-two male Sprague Dawley rats treated with BoNT/A (i.m., 1IU) were divided in four groups, depending on the time of BoNT/A injection (2 days before, 1, 2, and 4 weeks before the experiment). Bio-Plex Pro Rat Cytokine 23-plex Multiplex Assay (Bio-Rad, USA). Results Systemic inflammation: 17 cytokines (IL1-α ( p = 0.005), IL-1β ( p = 0.01), IL-2 ( p = 0.04), IL-4 ( p = 0.03), IL-6 ( p = 0.03), IL-10 ( p = 0.02), IL12(p70) ( p = 0.03), IL-13 ( p = 0.04), IL-17 ( p = 0.03), GM-CSF ( p = 0.03), INF-γ ( p = 0.03), MIP-1α ( p = 0.03), MIP-3α ( p = 0.04), RANTES ( p = 0.001), TNF-α ( p = 0.04), vascular endothelial growth factor ( p = 0.03), and MCP-1 ( p = 0.02)) showed significantly higher expression levels 2 days after intramuscular BoNT/A injections compared to other time points (1, 2, and 4 weeks). Local inflammation: 12 cytokines (IL-1β ( p = 0.02), IL-6 ( p = 0.002), IL-10 ( p = 0.02), IL-13 ( p = 0.04), IL-17 ( p = 0.02), TNF-α ( p = 0.001), GM-CSF ( p = 0.01), M-CSF ( p = 0.04), MIP-1α ( p = 0.04), MIP-3α ( p = 0.002), RANTES ( p = 0.02), and MCP-1( p = 0.004)) showed higher expression levels 2 and/or 4 weeks after intramuscular BoNT/A injections compared to the other time points (2 days and 1 week). Conclusion Intramuscular BoNT/A injections result in a rapid systemic inflammatory response that only lasts a couple of days. At the same time, intramuscular BoNT/A injections cause an inflammatory response locally in the muscle with significantly higher cytokine levels 2 and/or 4 weeks after injections