These responses were posture dependent, being greater in standing (soleus 57 %, FDB 67 % relative to pre-vibration) compared to sitting (soleus 36 %, FDB 27 % relative to pre-vibration) and leaning (soleus 26 %, FDB 8% relative to pre-vibration). After vibration offset, both soleus and FDB showed sustained activation across all three postures. Results highlight the presence of Ia afferent projections from the soleus to the α motor neurons of the FDB muscle triggered by Achilles' tendon vibration. This link is posture dependent serving a functional role in standing and forward leaning in the presence of externally applied perturbations.Novelty seems to reduce the persistence of aversive memories and to modulate frustration responses, yet much less is known on how this treatment affects memories lacking hedonic or emotional content. The present study analyzed how a 5-min exposure to a novel open field modulated the expression of a spatial recognition memory. Experiment 1 indicated that male Wistar rats trained in a T-maze in which one goal arm is blocked exhibit, when tested 2 h later, preference for the novel arm. This recognition memory was impaired by the muscarinic cholinergic antagonist scopolamine. Postraining, but not pretraining, novelty exposure rescued the cognitive impairment induced by scopolamine (Experiment 2 and 3). Pretraining open field exposure alleviated the lack of memory expression, induced by imposing a 6 h delay between training and testing (Experiment 4). The study shows that a very brief exposure to novelty can improve expression of a spatial, recognition memory, a modulation that - in the case of the pretraining novelty exposure -- emerges even in spite of cholinergic blockade. The present results are consistent with research suggesting that novelty exposure can be an effective, non-pharmacological, treatment to modulate memory expression.Transient receptor potential vanilloid 3 (TRPV3), a non-selective cation ion channel, is regulated by small molecules such as Ca2+ and calmodulin (CaM). Together with S100A4 (S100 calcium-binding protein family), is critical in cell proliferation and progression. Although TRPV3 has been proved to play a role in Ca2+ regulation and participate in Ca2+-related cellular processes, its molecular mechanism remains unclear. In this study, we found that TRPV3 and S100A4 were co-expressed in the same region of the cell, and surprisingly, the protein expression level of TRPV3 significantly increased with the overexpression of S100A4. Moreover, co-immunoprecipitation results showed that these two proteins could bind with each other. Functionally, we found that when S100A4 was simultaneously expressed in cells, more Ca2+ would be transferred into the cells through the TRPV3 ion channel. Consistent with Ca2+ regulation results, electrophysiological recordings demonstrated that S100A4 improved the function of TRPV3 in ions' flux, suggesting that the S100A4 could bind with TRPV3 and simultaneously promoted its expression, thus affecting its functions on related ions' flux. Our findings identified the link between S100A4 and TRPV3 and provided a novel molecular mechanism for TRPV3 regulation.Current available antidepressants have various adverse reactions and slow pharmacodynamics, so it is necessary to find novel antidepressants for effective treatment. Xanthoceraside (XAN), a novel triterpenoid saponin extracted from the fruit husks of Xanthoceras sorbifolium Bunge, has anti-amnesic and neuroprotective properties. The purpose and significance of this study is to assess whether XAN has antidepressant effects in mice using the forced swim test (FST), tail suspension test (TST) and chronic unpredictable mild stress (CUMS) model of depression. The effects of XAN treatment on the hippocampal brain-derived neurotrophic factor (BDNF) signaling pathway and neurogenesis were examined. The antidepressant mechanism of XAN was explored using a BDNF inhibitor (K252a) and an anti-BDNF antibody. It was found that XAN administration significantly reversed the depressive-like behaviors of CUMS-treated mice. XAN treatment also significantly prevented the decreasing effects of CUMS on the hippocampal BDNF signaling and neurogenesis. The antidepressant effects of XAN in mice were blocked by both administration of K252a and anti-BDNF antibody. Collectively, these findings indicate that XAN possesses antidepressant effects in mice which are mediated by activation of hippocampal BDNF signaling pathway, thus providing the first evidence that XAN can be a potential antidepressant candidate.Sex differences influence human and animal behavioral and pharmacological responses. The zebrafish (Danio rerio) is a powerful, popular model system in neuroscience and drug screening. Cell Cycle inhibitor However, the impact of zebrafish sex differences on their behavior and drug responses remains poorly understood. Here, we evaluate baseline anxiety-like behavior in adult male and female zebrafish, and its changes following an acute 30-min exposure to 800-μM scopolamine, a common psychoactive anticholinergic drug. Overall, we report high baseline anxiety-like behavior and more individual variability in locomotion in female zebrafish, as well as distinct, sex-specific (anxiolytic-like in females and anxiogenic-like in males) effects of scopolamine. Collectively, these findings reinforce the growing importance of zebrafish models for studying how both individual and sex differences shape behavioral and pharmacological responses.Type 2 diabetes mellitus (DM) is constantly increasing worldwide and its most critical determinant of morbidity and mortality is still represented by cardiovascular (CV) complications. For years, cardiologists' approach to diabetic patients has been focused on risk factors optimization, with positive results. However, the management of DM per se was never truly considered in order to obtain prevention from major CV events, because medications used for glycemic control were not expected to gain CV benefit. Early trials concerning intensive versus conventional glycemia control did not prove useful in reducing the number of CV events. The introduction of new molecules led to a game change in DM treatment, as some new glucose-lowering drugs (GLDs), such as sodium-glucose linked transporter-2 inhibitors (SGLT-2i) and glucagon-like peptide 1 receptor agonists (GLP-1 RA), showed not only to be safe but also to ensure CV benefit. A combination of anti-atherogenic effects and hemodynamic improvements are likely explanations of the observed reduction of CV events and mortality.