Neuroscience
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Signal processing in the principal neurons of the anteroventral cochlear nucleus (AVCN) is modulated by glycinergic inhibition. The kinetics of IPSCs are specific to the target neurons. It remains unclear what glycine receptor subunits are involved in generating such target-specific IPSC kinetics in AVCN principal neurons. ⋯ To further identify the cell type-specific expression patterns of GlyRα subunits, we combined whole-cell patch clamp recording with immunohistochemistry by recording from all three types of AVCN principal neurons, characterizing the synaptic properties of their glycinergic inhibition, dye-filling the neurons, and processing the slice for immunostaining of different GlyRα subunits. We found that AVCN bushy neurons express both GlyRα1 and GlyRα4 subunits that underlie their slow IPSC kinetics, whereas both T-stellate and D-stellate neurons express only GlyRα1 subunit that underlies their fast IPSC kinetics. In conclusion, AVCN principal neurons express cell-type specific GlyRα subunits that underlie their distinct IPSC kinetics, which enables glycinergic inhibition from the same source to exert target cell-specific modulation of activity to support the unique physiological function of these neurons.
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Stroke is a major life-threatening and disabling disease with a restricted therapeutic approach. Bone marrow stromal cells (BMSCs) possess proliferative ability and a multi-directional differentiation potential, and secrete a range of trophic/growth factors that can protect neurons after cerebral ischemia/reperfusion. Transient receptor potential canonical (TRPC) is a family of non-selective channels permeable to Ca2+, with several functions including neuronal survival. ⋯ In the present study, we report that over-expression of TRPC6 via a CRISPR-based synergistic activation mediator in BMSCs provided a greater reduction of brain injury in a rat model of ischemia/reperfusion. Further, the improved neurofunctional outcomes were associated with increased TRPC6 and brain derived neurotrophic factor expression levels. Overall, these data suggest that TRPC6 over-expressing BMSCs may be a promising therapeutic agent for ischemic stroke.