TRPM3 Channels Play Roles in Heat Hypersensitivity and Spontaneous Pain after Nerve Injury.

Transient receptor potential melastatin 3 (TRPM3) is a heat-activated ion channel in primary sensory neurons of the dorsal root ganglia (DRGs). Pharmacological and genetic studies implicated TRPM3 in various pain modalities, but TRPM3 inhibitors were not validated in TRPM3 mice. Here we tested two inhibitors of TRPM3 in male and female wild-type and TRPM3 mice in nerve injury-induced neuropathic pain.

The TRPM3 ion channel mediates nociception but not itch evoked by endogenous pruritogenic mediators.

During the molecular transduction of itch, the stimulation of pruriceptors on sensory fibers leads to the activation or sensitization of ion channels, which results in a consequent depolarization of the neurons. These ion channels mostly belong to the transient receptor potential (TRP) channels, which are involved in nociception and thermosensation. In particular, TRPV1 and TRPA1 were described in the transduction of both thermal nociception as well as histaminergic and non-histaminergic itch.

An electrostatically crosslinked chitosan hydrogel as a drug carrier.

Considerable efforts have been devoted to control and maintain the sustained release of proteins. In this experiment, we used bovine serum albumin-fluorescein isothiocyanate (BSA-FITC) as a model protein to explore the potential utility of a chitosan and glycerol phosphate disodium salt (GP) hydrogel as a protein drug depot. The mixing of chitosan and GP solutions (0, 10, 20 and 30 wt%) formed a liquid at room temperature.