Physiological consequences of a peptide cotransmitter in a crayfish nerve-muscle preparation

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Abstract
The pentapeptide proctolin is colocalized with a conventional, conductance-increasing neurotransmitter in 3 of 5 excitatory motoneurons that innervate a posture-related tonic flexor muscle of the crayfish. It is released from these neurons in response to nerve impulses. Nanomolar concentrations of proctolin superfused on the tonic flexor muscle act postsynaptically to potentiate tension generated by a given level of depolarization. Proctolin alone has no detectable effect on muscle tension, nor does it alter the resting membrane potential of the muscle. Proctolin produces no detectable effect on the EPSPs of the 1 proctolinergic motoneuron that was examined. Neurally released proctolin can be selectively depleted from severed motor axons following prolonged, low-frequency stimulation; EPSPs reflecting conventional transmitter release are unaltered by this procedure. After proctolin depletion, tension generated by the motoneuron is greatly reduced. Taken together, these results indicate that the peptide secondary transmitter in this neuromuscular preparation is an important contributor to the magnitude of tension generated by the motoneuron, but since its effect is dependent on the depolarizing EPSPs of the conventional neurotransmitter, it does not contribute to the temporal aspects of tension generation. These aspects are controlled exclusively by the conventional neurotransmitter.