I S Petropoulos, A E Jordan, P S Dickinson, D J Powell
{"title":"Peptidergic Modulation of the Lobster Cardiac System Has Opposing Action on Neurons and Muscles.","authors":"I S Petropoulos, A E Jordan, P S Dickinson, D J Powell","doi":"10.1093/iob/obaf002","DOIUrl":null,"url":null,"abstract":"<p><p>Modulation of neuronal networks, primarily through neuropeptides, generates variations in motor patterns that allow organisms to adapt to environmental changes or sensory inputs. Modulation is complex, with receptors for neuromodulators expressed at various locations within a nervous system; neuromodulators can thus alter muscle dynamics peripherally via the neuromuscular junction (NMJ) and the muscle itself. The neurogenic cardiac neuromuscular system of the American lobster (<i>Homarus americanus</i>) is a well-characterized model for investigating peptidergic modulation. Myosuppressin (pQDLDHVFLRFamide) is an endogenous peptide that interestingly decreases contraction frequency while also increasing contraction force by acting at both the lobster heart central pattern generator (CPG; the cardiac ganglion) and the periphery (cardiac muscles). Myosuppressin decreases heartbeat frequency by decreasing the burst frequency of the cardiac ganglion. Here, we investigated the remaining question, does myosuppressin exert its peripheral effects directly on the cardiac muscle, the NMJ, or both? To elucidate myosuppressin's effects on the cardiac muscle, the muscle was isolated from the CPG, and contractions were evoked using focal application of the endogenous neurotransmitter, l-glutamate, while superfusing myosuppressin over the heart. Myosuppressin increased glutamate-evoked contraction amplitude in the isolated muscle, suggesting that myosuppressin exerts its peripheral effects directly on the cardiac muscle. To examine effects on the NMJ, excitatory junction potentials were evoked by stimulating the motor nerve and recording the intracellular membrane voltage from a single muscle fiber both in control saline and in the presence of myosuppressin. Myosuppressin did not modulate the amplitude of excitatory junction potentials suggesting that myosuppressin acts directly on the muscle and not via the NMJ, to cause an increase in contraction force.</p>","PeriodicalId":13666,"journal":{"name":"Integrative Organismal Biology","volume":"7 1","pages":"obaf002"},"PeriodicalIF":2.2000,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11816307/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Integrative Organismal Biology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1093/iob/obaf002","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"BIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Modulation of neuronal networks, primarily through neuropeptides, generates variations in motor patterns that allow organisms to adapt to environmental changes or sensory inputs. Modulation is complex, with receptors for neuromodulators expressed at various locations within a nervous system; neuromodulators can thus alter muscle dynamics peripherally via the neuromuscular junction (NMJ) and the muscle itself. The neurogenic cardiac neuromuscular system of the American lobster (Homarus americanus) is a well-characterized model for investigating peptidergic modulation. Myosuppressin (pQDLDHVFLRFamide) is an endogenous peptide that interestingly decreases contraction frequency while also increasing contraction force by acting at both the lobster heart central pattern generator (CPG; the cardiac ganglion) and the periphery (cardiac muscles). Myosuppressin decreases heartbeat frequency by decreasing the burst frequency of the cardiac ganglion. Here, we investigated the remaining question, does myosuppressin exert its peripheral effects directly on the cardiac muscle, the NMJ, or both? To elucidate myosuppressin's effects on the cardiac muscle, the muscle was isolated from the CPG, and contractions were evoked using focal application of the endogenous neurotransmitter, l-glutamate, while superfusing myosuppressin over the heart. Myosuppressin increased glutamate-evoked contraction amplitude in the isolated muscle, suggesting that myosuppressin exerts its peripheral effects directly on the cardiac muscle. To examine effects on the NMJ, excitatory junction potentials were evoked by stimulating the motor nerve and recording the intracellular membrane voltage from a single muscle fiber both in control saline and in the presence of myosuppressin. Myosuppressin did not modulate the amplitude of excitatory junction potentials suggesting that myosuppressin acts directly on the muscle and not via the NMJ, to cause an increase in contraction force.