1. The action of serotonin on excitatory transmission in the opener muscle of the dactyl of the lobster walking leg was examined by intracellular recording techniques. 2. Serotonin, at concentrations as low as 5 x 10(‐9) M, caused a sustained increase in the size of the excitatory junctional (synaptic) potential (e.j.p.). When serotonin was washed out of the bath the e.j.p. declined in two steps (T 1/2 approximately equal to 1‐2 min; T 1/2 approximately equal to 30 min) to the control size. The increased e.j.p. size was predominantly due to a serotonin‐induced increase in the release of quanta of excitatory transmitter with nerve stimulation. 3. The increase in transmitter release did not require nerve stimulation or the presence of Na+ or Ca2+ ions in the bathing medium during the period of serotonin treatment. 4. Three types of experiments suggested that a part of the action of serotonin on excitatory nerve terminals might involve a long‐term metabolic change within terminals, possibly involving the buffering or storage of Ca2+ ions. First, serotonin increased the frequency of spontaneous release of transmitter in both normal saline (26 mM‐Ca2+) and saline with very low levels of Ca2+ (less than 10(‐8) M). Secondly, serotonin greatly potentiated increases in miniature excitatory junctional potential frequency induced by the loading of the nerve terminal with Na+ either by veratridine or by inhibition of the Na+ pump or by the addition of the Na‐ionophore monensin in low‐Ca2+ salines. Thirdly, in some experiments, serotonin treatment produced a partial restoration of the nerve‐evoked release of transmitter in the low‐Ca2+ medium (less than 10(‐8) M).

Sensory neuropathies, particularly trigeminal neuropathy, have been recognized as neurological complications of Sjögren's syndrome, but the pathogenesis has not been established. We describe a woman with primary Sjögren's syndrome who developed a progressive debilitating subacute sensory neuronopathy. Results of electrophysiological studies were consistent with involvement of the trigeminal and dorsal root ganglia. A thoracic dorsal root ganglion biopsy showed lymphocytic infiltration and degeneration of ganglion cells. We believe that this is the first description of biopsy-documented dorsal root ganglionitis in a subacute sensory neuronopathy associated with Sjögren's syndrome and that the finding suggests an immunopathogenic basis.