Extracellular K+ as an Interneuronal Coupler in the Carotid Body

Recent biophysical studies in the carotid body have shown that the membrane characteristics of type I cells (TICs) and type II cells (TIICs) fit those of a neuron and a glial cell, respectively (1). Other studies have shown also that, in addition to their ability to fire action potentials, TICs respond to cyanide with an increase in K+ conductance and a reversible increase in intracellular calcium (2,3). These results suggest that a neurotransmitter is released from TICs in hypoxia, as previously demonstrated in the whole carotid body (4). As a consequence, the interest in the “neurotransmitter hypothesis” to explain the coupling between TICs and nerve endings (NEs) has been revived recently. However, the main objections to the neurotranmitter hypothesis remain since no antagonist has been found yet that blocks the carotid body response to hypoxia, nor has a neurotransmitter been shown to induce sustained afferent discharge comparable to that seen in severe hypoxia (5).