A-kinase anchoring protein 79/150 coordinates metabotropic glutamate receptor sensitization of peripheral sensory neurons.

摘要: Glutamate serves as the primary excitatory neurotransmitter in nervous system. Previous studies have identified a role for glutamate and group I metabotropic receptors targets study peripheral inflammatory pain. However, coordination of signaling events that transpire from receptor activation to afferent neuronal sensitization has not been explored. Herein, we identify scaffolding protein A-kinase anchoring 79/150 (AKAP150) coordinates increased thermal sensitivity after (mGluR5) activation. In both acute persistent models somatosensory behavior, report mGluR5 requires AKAP150 expression. Furthermore, electrophysiological approaches designed record activity reveal also functional dissociated neurons, increases TRPV1 responses an AKAP-dependent manner through mechanism induces AKAP association with TRPV1. Experimental results presented herein receptor-driven ion channel targets. Importantly, this could prove significant search therapeutic repress episodes pain becoming chronic nature.