Peptide and amine transmitter effect on embryonic chick sensory neurons in vitro

It has been known for some time that NE and ACh can affect voltage-sensitive channels in the heart but it has only recently been appreciated that neurotransmitters (and certain peptides) can modulate voltage-sensitive channels in neurons. In addition to the effect on the action potential of embryonic chick sensory neurons described here, NE decreases the duration of spikes in rat superior cervical ganglion neurons (7). Serotonin prolongs action potentials recorded in Aplysia sensory neurons (9) and an as yet unidentified transmitter decreases an inward Ca++ current in the same cells (20). In the heart, one important consequence of the effect of NE and ACh on the action potential is a change in the strength and/or duration of contraction. In neurons, attention has been focused on the possibility that modulation of voltage-sensitive channels might result in a change in transmitter release. In Aplysia, the 5-HT induced prolongation of sensory neuron some spikes is associated with a dramatic augmentation of transmitter release at sensory nerve-motorneurone synapses (9) and the decrease in some inward Ca++ current is associated with presynaptic inhibition (20). Enkephalin, NE, GABA, and 5-HT can inhibit the evoked release of Substance P from cultured embryonic chick sensory neurons. These same drugs decrease ICa, apparently by decreasing the number of the conductance of voltage-sensitive Ca++ channels. The two phenomena may be related. It is significant in this regard that the same variability (between platings) in the ability of enkephalin to reduce Substance P release was also observed in the effect of enkephalin on action potential duration. Cells that released normal amounts of Substance P in the presence of enkephalin also exhibit spikes of normal duration in the presence of the peptide.