Growing pains: the cytoskeleton as a critical regulator of pain plasticity.
Inflammatory mediators act on peripheral sensory neurons to produce pain and hypersensitivity after tissue injury. In this issue of Neuron, Dina et al. report that inflammatory mediators, such as epinephrine and prostaglandins, appear to couple to specific G protein-coupled receptor signaling pathways through plastic interactions with the cytoskeleton.
Bhave
Gautam
G
Division of Neuroscience, Baylor College of Medicine, Houston, TX 77030, USA.
Gereau
Robert W
RW
D000818:Animals; D003599:Cytoskeleton / Q000502:physiology*; D015232:Dinoprostone / Q000378:metabolism; D004837:Epinephrine / Q000378:metabolism; D009473:Neuronal Plasticity / Q000502:physiology*; D009475:Neurons, Afferent / Q000502:physiology; D009619:Nociceptors / Q000502:physiology; D010146:Pain / Q000503:physiopathology*; D019707:Receptors, Chemokine / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology*
D019707:Receptors, Chemokine; D015232:Dinoprostone; D004837:Epinephrine