Synchronous Infra-Slow Oscillations Organize Ensembles of Accessory Olfactory Bulb Projection Neurons into Distinct Microcircuits

The accessory olfactory system controls social and sexual behavior. In the mouse accessory olfactory bulb, the first central stage of information processing along the accessory olfactory pathway, projection neurons (mitral cells) display infra-slow oscillatory discharge with remarkable periodicity. The physiological mechanisms that underlie this default output state, however, remain controversial. Moreover, whether such rhythmic infra-slow activity patterns exist in awake behaving mice and whether such activity reflects the functional organization of the accessory olfactory bulb circuitry remain unclear. Here, we hypothesize that mitral cell ensembles form synchronized microcircuits that subdivide the accessory olfactory bulb into segregated functional clusters. We use a miniature microscope to image the Ca2+ dynamics within the apical dendritic compartments of large mitral cell ensembles in vivo. We show that infra-slow periodic patterns of concerted neural activity, indeed, reflect the idle state of accessory olfactory bulb output in awake male and female mice. Ca2+ activity profiles are distinct and glomerulus-specific. Confocal time-lapse imaging in acute slices reveals that groups of mitral cells assemble into microcircuits that exhibit correlated Ca2+ signals. Moreover, electrophysiological profiling of synaptic connectivity indicates functional coupling between mitral cells. Our results suggest that both intrinsically rhythmogenic neurons and neurons entrained by fast synaptic drive are key elements in organizing the accessory olfactory bulb into functional microcircuits, each characterized by a distinct default pattern of infra-slow rhythmicity

Magnetic Stimulation Therapy in Patients with COPD: A Systematic Review

Magnetotherapy (MT) is a therapeutic treatment based on the use of magnetic fields (MF) that can have an anti-inflammatory and analgesic effect. MT represents a possible treatment or an ancillary therapeutic intervention for a wide range of diseases and it is often used in the field of physiotherapeutic practices. A crucial point in the treatment of chronic obstructive pulmonary disease (COPD) patients, to counteract muscular depletion and respiratory symptoms, is represented by physiotherapy. Nevertheless, the knowledge about the application of MF as a therapeutic option in COPD patients is very limited. The purpose of the present study was to define what is currently known about the use of MF in patients with COPD. A systematic review of the literature was conducted during the month of October 2017, searching three main databases. Only those citations providing detailed informations about the use of MF to treat COPD symptoms either during an acute or a chronic phase of the disease, were selected. Following the selection process three articles were included in the final analysis. The present review focused on a total of thirty-six patients with COPD, and on the effects of the application of MF. In the majority of cases, the treatment sessions with MF were carried-out in an outpatient setting, and they differed with regard to the duration; frequency of application; dosage; intensity of the applied MF. Basing on the available informations, it seems that MF is a feasible, well tolerated, safe therapeutic option, for the treatment of motor-related COPD symptoms

Coagulation, Protease-Activated Receptors, and Viral Myocarditis

The coagulation protease cascade plays an essential role in hemostasis. In addition, a clot contributes to host defense by limiting the spread of pathogens. Coagulation proteases induce intracellular signaling by cleavage of cell surface receptors called protease-activated receptors (PARs). These receptors allow cells to sense changes in the extracellular environment, such as infection. Viruses activate the coagulation cascade by inducing tissue factor expression and by disrupting the endothelium. Virus infection of the heart can cause myocarditis, cardiac remodeling and heart failure. Recent studies using a mouse model have shown that tissue factor, thrombin and PAR-1 signaling all positively regulate the innate immune during viral myocarditis. In contrast, PAR-2 signaling was found to inhibit interferon-β expression and the innate immune response. These observations suggest that anticoagulants may impair the innate immune response to viral infection and that inhibition of PAR-2 may be a new target to reduce viral myocarditis.