Pharmacological studies have revealed that the effects of certain putative neurotransmitters on peripheral neurons in autonomic and sensory ganglia are very similar to the effects of these agents on primary afferent terminals in the central nervous system1,2, 4 15,17,18,23,34. Thus it was suggested that peripheral ganglia might be useful model systems for examining the 'presynaptic' actions of drugs 4,1°-1~A7. In this regard it was shown that gamma-aminobutyric acid (GABA) a transmitter which hyperpolarizes central nerve cells 6 depolarizes peripheral ganglion cells and primary afferent terminalsl,2,4-15,1s, 34. The depolarizing responses were blocked by picrotoxin and bicuculline, agents which also block neurally-evoked primary afferent depolarization and presynaptic inhibition in the spinal cord5-7A6,e4, 31. These observations provided support for the view that GABA was a presynaptic inhibitory transmitter. The present investigation was undertaken to study the response of sensory ganglion cells to 5-hydroxytryptamine (5-HT), a substance that has also been implicated in presynaptic inhibition in the spinal c0rd3,27,29,~2,~, 36. It is well known that 5-HT depolarizes and excites afferent nerves as well as peripheral ganglion cells14,2°,e5,26,28,a°, 35. In autonomic ganglia its excitatory effects are blocked by picrotoxin14, 30. The present experiments demonstrate that picrotoxin also blocks the excitatory effects of 5-HT on afferent neurons in the nodose ganglion and afferent axons in the carotid sinus nerve. Experiments were performed on 14 cats anesthetized with a mixture of diallylbarbiturate (70 mg/kg), urethane (280 mg/kg) and monoethylurea (280 mg/kg). After intubation of the trachea, the nodose ganglion, the carotid sinus nerve and vagus nerve on the left side were dissected free from underlying connective tissue. Potentials were recorded from the surface of the ganglion with silver-silver chloride electrodes connected to a resistance-coupled preamplifier. One electrode was placed in direct