Sensory neuron sensitivity is modulated by a large variety of mediators that can activate a plethora of signaling cascades. These signaling cascades allow sensory neurons to show remarkable plasticity in response to injury and inflammation. The understanding of intracellular signaling mechanisms that regulate sensory neuron function downstream of receptor–ligand interactions or electrical activity is still at a relatively developing stage. This article highlights what is known about some of the components of classical intracellular signal transduction cascades, such as cyclic adenosine monophosphate (cAMP) and downstream cAMP sensors, mitogen-activated protein kinases, and others in regulating sensory neuron function. How these transduction cascades may contribute to the initiation, maintenance, or even resolution of inflammatory and neuropathic pain is discussed. Moreover, the focus is on how intracellular signaling cascades themselves are subject to plasticity and how this plasticity may underlie the development of chronic pain.
microRNA-dependent control of sensory neuron function regulates posture behaviour in Drosophila
