Mechanosensation - Cutaneous Mechanoreceptors - Molecular Mechanisms

Molecular Mechanisms

Known molecular mechanisms of cutaneous mechanosensitivity are not completely understood. Most likely, a single unifying transduction process by which all sensory neurons function does not exist. It is believed, however, that sensory neurons employ fast, mechanically gated cation channels, and that the depolarization that results across the membrane is followed by the generation of a sodium-dependent action potential at the transduction site. It is believed that rapid, mechanically gated cation channels are characteristic of all sensory neurons. The membrane depolarization, in turn, leads to a sodium-dependent action potential at that location. It is also thought that mechanical strain is detected by ion channels through cytoplasmic and extracellular components. The existence of a distinct transduction process for all sensory neurons is highly unlikely. It has been hypothesized that the attachment of ion channels to cytoplasmic and extracellular structures is responsible for distinguishing mechanical strain on the cell membrane, and that cell curvature may not directly gate these ion channels alone. Mechanosensation also contributes to cell growth and development through extracellular matrix (ECM) interaction and traction of integrin receptors which facilitate adhesion.