Plasticity of vagal afferent fibres mediating cough

Increased sensitivity of cough pathways has been demonstrated in numerous studies. The underlying mechanisms of this sensitization are largely unknown; however, a burgeoning body of evidence suggests that vagal primary afferent neurones that innervate the airways are likely to be involved. This plasticity includes changes in anatomy, neurochemistry and function. PGE2 is an example of an inflammatory mediator that increases responsiveness to tussive stimuli. Electrophysiological studies of neurone cell bodies isolated from afferent ganglia have revealed that prostanoids modulate the function of a variety of distinct ion channels including those that carry TTX-insensitive voltage-gated sodium currents, slow post-spike hyperpolarizations and a hyperpolarization-activated cation current. Mediator-induced modulation of the function of various voltage-gated currents operating at the peripheral terminals of airway afferent neurons would probably influence input from the airways into the central nervous system and contribute to the urge to cough and increased responsiveness to tussive stimuli.