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Metabotropic glutamate receptor 5 (mGluR5) has been implicated in stress-related psychiatric disorders, particularly major depressive disorder. Although growing evidence supports the proresilient role of mGluR5 in corticolimbic circuitry in the depressive-like behaviors following chronic stress exposure, the underlying neural mechanisms, including circuits and molecules, remain unknown.We measured the c-Fos expression and probability of neurotransmitter release in and from basolateral amygdala (BLA) neurons projecting to the medial prefrontal cortex (mPFC) and to the ventral hippocampus (vHPC) after chronic social defeat stress. The role of BLA projections in depressive-like behaviors was assessed using optogenetic manipulations, and the underlying molecular mechanisms of mGluR5 and downstream signaling were investigated by Western blotting, viral-mediated gene transfer, and pharmacological manipulations.Chronic social defeat stress disrupted neural activity and glutamatergic transmission in both BLA projections. Optogenetic activation of BLA projections reversed the detrimental effects of chronic social defeat stress on depressive-like behaviors and mGluR5 expression in the mPFC and vHPC. Conversely, inhibition of BLA projections of mice undergoing subthreshold social defeat stress induced a susceptible phenotype and mGluR5 reduction. These two BLA circuits appeared to act in an independent way. We demonstrate that mGluR5 overexpression in the mPFC or vHPC was proresilient while the mGluR5 knockdown was prosusceptible and that the proresilient effects of mGluR5 are mediated through distinctive downstream signaling pathways in the mPFC and vHPC.These findings identify mGluR5 in the mPFC and vHPC that receive BLA inputs as a critical mediator of stress resilience, highlighting circuit-specific signaling for depressive-like behaviors.

Robotic manipulators require contact force sensing capabilities to sense the contact force between the manipulator and an object. Specifically, for humans and robots to coexist in the work environment, the robot must be able to detect an external force applied by a human. This study presents a new intrinsic force sensing method for robot manipulators that can obtain accurate information of the external force applied by a human during human–robot interaction. The method employs a robot cover, which is typically utilized in robot manipulators. Unlike conventional force sensing methods, a six-axis force/torque sensor is placed between the cover and the link of the robot manipulator. As a result, the proposed method provides information of the three-axis contact force applied to the cover surface and its contact location. Therefore, the cover itself becomes a sensorized cover based on the intrinsic force sensing method. To evaluate its sensing performance, the sensorized cover is experimentally validated using reference sensors. Finally, an experiment is performed in which the robot successfully recognizes letters written on the cover, indicating a high level of contact force sensing performance.

SummarySocial animals compete for limited resources, resulting in a social hierarchy. Although different neuronal subpopulations in the medial prefrontal cortex (mPFC), a hub brain region of social hierarchy, encode distinct social competition behaviors, their identities and associated molecular underpinnings have not yet been identified. In this study, we found that mPFC neurons projecting to the nucleus accumbens (mPFC-NAc) encode social winning behavior, whereas mPFC neurons projecting to the ventral tegmental area (mPFC-VTA) encode social losing behavior by monitoring and manipulating neural circuit activity. High-throughput single-cell transcriptomic analysis and projection-specific genetic manipulation revealed that the expression level of POU domain, class 3, transcription factor 1 (Pou3f1) in mPFC-VTA neurons controls social hierarchy. Optogenetic activation of mPFC-VTA neurons increasesPou3f1expression and lowers social rank. Together, these data demonstrate that discrete activity and gene expression in separate mPFC projections oppositely orchestrate social competition and hierarchy.

Many synaptic adhesion molecules positively regulate synapse development and function, but relatively little is known about negative regulation. SALM4/Lrfn3 (synaptic adhesion-like molecule 4/leucine rich repeat and fibronectin type III domain containing 3) inhibits synapse development by suppressing other SALM family proteins, but whether SALM4 also inhibits synaptic function and specific behaviors remains unclear. Here we show that SALM4-knockout (Lrfn3−/−) male mice display enhanced contextual fear memory consolidation (7-day post-training) but not acquisition or 1-day retention, and exhibit normal cued fear, spatial, and object-recognition memory. The Lrfn3−/− hippocampus show increased currents of GluN2B-containing N-methyl-d-aspartate (NMDA) receptors (GluN2B-NMDARs), but not α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors (AMPARs), which requires the presynaptic receptor tyrosine phosphatase PTPσ. Chronic treatment of Lrfn3−/− mice with fluoxetine, a selective serotonin reuptake inhibitor used to treat excessive fear memory that directly inhibits GluN2B-NMDARs, normalizes NMDAR function and contextual fear memory consolidation in Lrfn3−/− mice, although the GluN2B-specific NMDAR antagonist ifenprodil was not sufficient to reverse the enhanced fear memory consolidation. These results suggest that SALM4 suppresses excessive GluN2B-NMDAR (not AMPAR) function and fear memory consolidation (not acquisition)., To elucidate the role of synaptic cell adhesion-like molecule 4 (SALM4) in altering synaptic function in the context of fear memory, Lie at al performed behavioural and electrophysiological assessments of SALM4 knockout mice undergoing cued fear, spatial, and object-recognition memory tasks. They demonstrated that SALM4 suppresses heightened GluN2B-expressing NMDA receptor function specifically during fear memory consolidation.

In this paper, we propose a robust method for estimating the parameters of robot manipulators using the torque separation technique, which was developed previously by the authors, to extract the inertial, gravitational, and frictional components from the input torques of multiple sinusoidal joint motions. The separated components of the input torque produce a set of reduced linear regression equations where the dynamic parameters of the robot manipulators appear decoupled or minimally coupled. A mathematical analysis is presented to show that the set of reduced regression equations tends to yield more robust parameter estimation than the conventional way where a large dimensional full regression equation is solved simultaneously. An iterative scheme to alleviate the possibility of parameter estimation error caused by the deviation from the assumed ideal sinusoidal motions is also proposed. Experimentation with two robot manipulators is used to verify the proposed approach and related claims. The proposed method is simple and pragmatic without requiring any specialized signal filtering and technical know-hows which numerous previous methods often demanded for explicitly or implicitly.

Often called the second brain, the gut communicates extensively with the brain and vice versa. The conversation between these two organs affects a variety of physiological mechanisms that are associated with our mental health. Over the past decade, a growing body of evidence has suggested that the gut microbiome builds a unique ecosystem inside the gastrointestinal tract to maintain the homeostasis and that compositional changes in the gut microbiome are highly correlated with several mental disorders. There are ongoing efforts to treat or prevent mental disorders by regulating the gut microbiome using probiotics. These attempts are based on the seminal findings that probiotics can control the gut microbiome and affect mental conditions. However, some issues have yet to be conclusively addressed, especially the causality between the gut microbiome and mental disorders. In this review, we focus on the mechanisms by which the gut microbiome affects mental health and diseases. Furthermore, we discuss the potential use of probiotics as therapeutic agents for psychiatric disorders.