Effect of sodium perturbations on rat chemoreceptor spike generation: implications for a Poisson model

The sensitivity of arterial chemoreceptor spike generation to reductions in excitability was examined using rat chemoreceptors in vitro. Axonal excitability was reduced by reducing extracellular sodium concentration ([Na + ] o ) by 10-40 % or by applying low doses of tetrodotoxin (TTX). In normoxia and in hypoxia, an isosmotic reduction in [Na + ] o caused a proportional decrease in single-fibre, spiking nerve activity. For a 20 % reduction in [Na + ] o , nerve activity decreased to 54 ± 7 % of control in normoxia and 41 ± 5 % in hypoxia. Low doses of TTX (25-50 nM) caused a similar decrease in spiking frequency, but this response was variable amongst fibres, with some fibres unaffected by TTX. A reduction in [Na + ] o by 20 % caused a slowing of conduction velocity, measured using an electrical stimulus delivered to an electrode placed in the carotid body. Threshold current for spike generation was increased by about 2·7 ± 1·4 %. Threshold current increased by 6·5 ± 3·7 % following a 40 % reduction in [Na + ] o . The spike generation process was modelled as a Poisson process in which depolarizing events summate and give rise to an action potential. The experimental data were best fitted to a high order process characterized by a large number of events and high event threshold. This result is not consistent with depolarization events caused by episodic transmitter release, but suggests that afferent spike generation is an endogenous process in the afferent nerve fibres, perhaps linked to random channel activity or to thermal noise fluctuations.