Topic: β-adrenergic receptors

Neurons express a variety of G protein coupled receptors (GPCRs), which profoundly condition neuronal physiology by activating intracellular signalling cascades in response to extracellular signals, including neuromodulators such as noradrenaline and dopamine. One mechanism GPCR use to tune their activity is membrane trafficking. Upon ligand binding, GPCRs are endocytosed through distinct mechanisms via interaction with different proteins (e.g clathrin, endophilin). Moreover, endocytosis is affected by membrane composition. With the aim of studying endocytosis at single event level in living c

Altered neuronal excitability and synaptic inputs to motoneurons are part of the pathophysiology of Amyotrophic Lateral Sclerosis. The cAMP/PKA pathway regulates both of them but therapeutic interventions at this level are limited by the lack of knowledge about suitable pharmacological entry points. Here we used transcriptomics on microdissected and in situ motoneurons to reveal the modulation of PKA-coupled receptorome in SOD1(G93A) ALS mice, vs WT, demonstrating the dysregulation of multiple PKA-coupled GPCR, in particular on vulnerable MN, and the relative sparing of β-adrenergic. In vivo M