Thermally induced neuronal plasticity in the hypothalamus mediates heat tolerance.

Heat acclimation is an adaptive process that improves physiological performance and supports survival in the face of increasing environmental temperatures, but the underlying mechanisms are not well understood. Here we identified a discrete group of neurons in the mouse hypothalamic preoptic area (POA) that rheostatically increase their activity over the course of heat acclimation, a property required for mice to become heat tolerant. In non-acclimated mice, peripheral thermoafferent pathways via the parabrachial nucleus activate POA neurons and mediate acute heat-defense mechanisms.

High-Resolution Melting PCR as a Fast and Simple Molecular Biology-Based Method for the Identification of Hypervirulent Strains Directly in Stool Samples.

became one of the main causes of nosocomial infections in all clinical settings worldwide, especially among patients undergoing antibiotic therapy. The incidence and severity of infections, from mild diarrhea to life-threatening pseudomembranous colitis, correlate with the spread of the hypervirulent binary toxin (CDT)-producing strains. The use of the real-time HRM-PCR method enables the identification of hypervirulent strains directly in the diarrheal stool samples of patients suspected of being infected with this bacterium.

Neuron-astrocyte metabolic coupling facilitates spinal plasticity and maintenance of inflammatory pain.

Long-lasting pain stimuli can trigger maladaptive changes in the spinal cord, reminiscent of plasticity associated with memory formation. Metabolic coupling between astrocytes and neurons has been implicated in neuronal plasticity and memory formation in the central nervous system, but neither its involvement in pathological pain nor in spinal plasticity has been tested. Here we report a form of neuroglia signalling involving spinal astrocytic glycogen dynamics triggered by persistent noxious stimulation via upregulation of the Protein Targeting to Glycogen (PTG) in spinal astrocytes.

TRPM4 keeps up the pace.

The study by Li et al., provides a detailed pharmacological characterization of the ionic mechanisms that underlie rhythmic activity of retrotrapezoid nucleus neurons that control breathing. Specifically, the authors demonstrate a role of the transient receptor potential melastatin 4 (TRPM4) ion channel in the generation of subthreshold excitatory oscillations.

SAP97-mediated rescue of NMDA receptor surface distribution in a neuronal model of Huntington's disease.

Huntington's disease (HD) is a genetic neurodegenerative disorder caused by an expansion of the CAG repeat tract in the HTT gene, leading to motor, cognitive, and psychiatric symptoms. At the cellular level, NMDA-type glutamate receptors are upregulated at glutamatergic extrasynaptic sites in HD, triggering cell death signaling pathways and driving HD neurodegeneration. Extrasynaptic and synaptic glutamate receptor trafficking and surface distribution are regulated by the α and β N-terminal isoforms of SAP97, a postsynaptic density protein localized at glutamatergic synapses.