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The evidence presented in the preceding three papers indicates that in all probability the carotid body chemoreceptors form a sensory synapse with a presynaptic element (presumably the glomus cells) and a postsynaptic element, namely, the sensory nerve endings (cf. also de Castro, 1951). The preceding studies also indicate that chemoreceptor impulses may be elicited by a substance (or substances) released from glomus tissues during stimulation. These agents have been tentatively designated as 'generator' or 'transmitter' substances. During some forms of stimulation (induced by hypoxia, hypercapnia and electrical stimulation) release of acetylcholine (ACh) or a similar substance seems to be responsible for the initiation of the chemosensory discharge. During stimulation induced by receptor exposure to N2, to NaCN or by interruption of flow, chemicals other than ACh may be released as well (Eyzaguirre & Koyano, 1965a,b,c).In order to establish the existence of chemical generation of sensory impulses it is important to know: (i) the nature and content of possible transmitter substances in carotid body tissues; (ii) whether or not such substances are released during stimulation and whether these activate sensory nerve endings. These problems were partly resolved in the present study. In the first place, ACh was found in carotid body tissues in sufficient quantities to be considered as a possible chemical transmitter during certain forms of stimulation. Secondly, chemicals were released by either electrical or 'natural' stimulation and these substances activated another chemoreceptor preparation placed in series. The nature of the released agent(s) remained undetermined.

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1. The carotid body and its nerve, removed from anesthetized cats, were placed in physiological saline flowing under paraffin oil. The nerve, lifted into the oil, was used for either electrical stimulation or recording of the total afferent discharge. Intracellular recordings were obtained from individual nerve fibers and endings within the carotid body. The recording sites were identified by injecting Procion yellow through the intracellular electrodes; the tissues were then prepared for histology and observed with episcopic fluorescence or Nomarski optics. 2. Intracellularly recorded chemosensory fibers conducted at 1.1-30 m/s and usually displayed action potentials of regular amplitude. At times, however, some spikes become partially blocked while others maintained their original amplitude. "Natural" (hypoxia) or chemical (ACh or NaCN) stimulation induced different patterns of frequency changes of the large and small action potentials. This indicated nerve fiber branching at some distance from the recording site. 3. Intra- and extracellularly recorded spikes were blocked in 0 [Na+]0 by tetrodotoxin (TTX) or procaine. 4. During chemical stimulation, a slowly occurring depolarization (receptor or generator potential) was recorded intracellularly from the afferent fibers. It developed concomitantly with the increase in discharge. 5. Impalement of single nerve terminals (histologically identified) showed numerous "spontaneous" depolarizing potentials (SDPs) that had a mean amplitude of 5.6 mV, a mean duration of 46.1 ms, and nearly random distribution. They increased in frequency and summated during chemical stimulation. SDPs originated from either the site of recording or from neighboring areas. When the SDPs attained a certain amplitude, they seemed to give rise to action potentials. Also, relatively well developed or partially blocked spikes (apparently originating elsewhere) were recorded from single nerve terminals. 6. The receptor (generator) potential of chemosensory receptors appears to be an integrated response formed by multiple activity originating in different nerve endings.