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Neurotransmitters decrease the calcium component of sensory neurone action potentials


RELEASE of neurotransmitters from presynaptic axon terminals requires the influx of Ca2+ ions during the nerve terminal action potential1. Action potentials recorded in some neurone cell bodies exhibit a relatively large Ca2+ component, and it has been suggested that these soma Ca2+ spikes may provide a model for Ca2+ influx across the less accessible nerve terminal membrane2. Recent data support the usefulness of this model. Serotonin (5-hydroxytryptamine, 5-HT) increases transmitter output at certain habituated sensory nerve-motoneurone synapses in the abdominal ganglion of Aplysia and it also prolongs the Ca2+ spike recorded in the sensory neurone cell body3. Enkephalin reduces the stimulated release of substance P by adult cat trigeminal neurones4 and by cultured embryonic chick dorsal root ganglion (DRG) neurones5, and it decreases the quantal content of excitatory postsynaptic potentials (, transmitter unknown) evoked in cultured rat spinal cord neurones by co-cultured DRG cells6. This peptide also decreases the duration and magnitude of the Ca2+ component of the DRG soma spike5. With the thought that modulation of Ca2+ currents may be a general correlate of presynaptic inhibition, we have studied the effect of several putative neurotransmitters on the soma spike of cultured chick sensory neurones, and report here that they decrease the calcium component of cell body action potentials.

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DUNLAP, K., FISCHBACH, G. Neurotransmitters decrease the calcium component of sensory neurone action potentials. Nature 276, 837–839 (1978).

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