The mammalian somatosensory system detects thermal, chemical, and mechanical stimuli. While some of the genes that mediate thermal and chemical stimuli have been identified, the molecular transducers of mechanical stimuli are still largely unknown, and represent one of the highest priorities in touch and pain biology. We carried out an unbiased screen and identified the ion channel Cyclic Nucleotide-Gated channel A2 (CNGA2) as a candidate transducer of touch stimuli. The goal of this proposal is to probe the role of CNGA2 in mechanotransduction in somatosensory neurons, the cells that mediate our sense of touch and pain. We will directly test the hypothesis that CNGA2 plays a key role in touch and/or pain using cellular, behavioral and genetic tools. The outcomes of this research will provide a better understanding of the transduction mechanisms underlying our sense of touch and pain, and may provide insight into new therapies and drugs to treat mechanical hypersensitivity that accompanies a wide range of neurological diseases.
Chronic pain and increased sensitivity to touch are features of numerous neurological disorders, such as peripheral neuropathies, neuralgia, fibromyalgia, multiple sclerosis, and certain migraines. In vertebrates, the sensation of touch and pain is initiated by a group of specialized neurons that detect mechanical, thermal, and chemical stimuli. The quest for the genes that mediate mechanical stimuli is still open, and represents one of the highest priorities in pain and touch research.