Of all the sensory modalities possessed by vertebrates, the ability to sense mechanical force remains the least well understood at the cellular and molecular level. In the glabrous skin, touch is sensed by Meissner and Pacinian corpuscles ? the detectors of fine objects and minute skin deformations. The corpuscles are innervated by rapidly-adapting neuronal mechanoreceptors, which can directly convert touch into excitation, by an unknown mechanism. Here, we aim to elucidate this mechanism by studying the mechanosensitivity in rapidly-adapting mechanoreceptors, using the trigeminal system of the duck embryo as a model. Duck trigeminal ganglia contain a large proportion of rapidly-adapting mechanoreceptors, which innervate the numerous Meissner- and Pacinian-like corpuscles in the glabrous skin of the bill. Using this model, we aim to determine the role of stretch-sensitive cationic and voltage-sensitive sodium channels in the three principal processes of touch sensitivity: (1) the conversion of touch into excitatory current; (2) the generation of action potential, and (3) propagation of the rapidly-adapting afferent message along the axon. Our studies will reveal cellular and molecular principles underlying the sense of touch in rapidly-adapting neuronal mechanoreceptors.
The sense of touch is a fundamental physiological capacity which allows us to interact with the environment through the perception of mechanical force. Our work will elucidate how mechanical force is perceived at the molecular level by neuronal mechanoreceptors. The proposed studies will obtain fundamental knowledge that will facilitate the development of novel pharmacological strategies to treat a range of neurological disorders associated with painful sensitivity in the skin.
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