Transduction mechanisms in carotid body: glomus cells, putative neurotransmitters, and nerve endings

Abstract

Carotid body chemoreceptors are activated by low PO2, high PCO2, acidity, increased temperature, and tonicity. These receptors are important in homeostasis and mediate their reflex effects on the CNS through sensory discharges of the carotid (sinus) nerve. The receptor complex is formed by glomus (type I) cells and carotid nerve endings, which, morphologically, appear to form a sensory synapse. The junction between glomus cells and nerve endings is enveloped by processes of sustentacular (type II) cells. The mechanisms of chemoreceptor transduction are complex; there is no agreement about the identity of the primary receptor element (glomus cell or nerve terminal) or what mechanisms are responsible for the onset of the sensory discharge in the carotid nerve. There is increasing evidence that integrity of the glomus cell is essential for normal transduction and that the receptor synapse described by morphologists may be functionally active. There is no conclusive evidence, however, that the glomus cell is the primary site of sensory transduction. Stimuli act on the glomus cell to release "transmitter" and/or "modulator" substances; but it is unknown if the released chemicals are directly responsible for the accompanying change in sensory impulse frequency or merely modify an already ongoing discharge. Interactions between glomus cells and nerves may be complicated enough to make it very difficult to resolve this question.