Determining the sites at which neuromodulators exert peripheral effects in the cardiac neuromuscular system of the American Lobster, Homarus americanus

Networks of neurons known as central pattern generators (CPGs) generate rhythmic patterns of output to drive behaviors like locomotion. CPGs are relatively fixed networks that produce consistent patterns in the absence of other inputs. The heart contractions of the Homarus americanus are neurogenic and controlled by the CPG known as the cardiac ganglion. Neuromodulators can enable flexibility in CPG motor output, and also on muscle contractions by acting on the neuromuscular junction and the muscle itself. A tissue-specific transcriptome gleaned from the cardiac ganglion and cardiac muscle of the American lobster was used to predict the sites and sources of a variety of crustacean neuromodulators. If corresponding receptors were predicted to be expressed in the cardiac muscle, then it was hypothesized that the neuropeptide had peripheral effects. One peptide for which a cardiac muscle receptor was identified is myosuppressin. Myosuppressin has been shown to have modulatory effects at the cardiac neuromuscular system of the American lobster. In previous research, myosuppressin had modulatory effects on the periphery of cardiac neuromuscular system alone. It remains an open question of whether myosuppressin acts on the cardiac muscle directly, if it is exerting its effects at the neuromuscular junction (NMJ), or both. To test this, I performed physiological experiments on the isolated NMJ. Myosuppressin did not modulate the amplitude of the excitatory junction potentials. Since no modulatory effects were seen at the NMJ, the cardiac muscle was isolated from the cardiac ganglion and then glutamate-evoked contractions were stimulated. I showed that myosuppressin increased glutamate-evoked contraction amplitude. These data suggest myosuppressin exerts its peripheral effects at the cardiac muscle and not the NMJ.