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Date: 2024-01-01

Creator: Andre Eden

Access: Open access

During every second of a human’s life, the cardiovascular system is modulated by factors both intrinsic and extrinsic to the physiology of the heart. We can uncover new insights regarding the nature of our system through investigations of similar systems in other model species. One example materializes itself in the form of the American Lobster (Homarus americanus) whose single-chambered heart finds resemblance to the function and anatomy to that of humans. The lobster heart is powered by the cardiac ganglion (CG), a group of neurons that drive contractions of surrounding heart muscles, known as the myocardium. Both the CG and myocardium work in a feedback loop, with both intrinsic (afterload and preload) and extrinsic (temperature and neuropeptides) factors affecting cardiac output (CO) or the overall ability of the heart to carry out its primary function of nutrient distribution. In this paper, we examine how the addition of these factors into in vitro whole heart preparations affect CO and other associated variables. From experimentation, we conclude that the neuropeptide SGRNFLRFamide (SGRN) increases the heartbeat frequency and the active force exerted by the heart. We also conclude that increases in temperature decrease CO as higher temperatures decrease heartbeat frequency and the active force exerted by the heart. Lastly, we conclude that the effect of preload and afterload combined produce more robust effects on the CO and active force of the heart, potentially painting a better picture of what may happen in vivo.

Date: 2023-01-01

Creator: Kenneth Garcia

Access: Open access

Neuromodulation allows for the flexibility of neural circuit dynamics and the outputs they produce. Studies of the stomatogastric nervous system (STNS) have expanded our knowledge on the actions of neuromodulators, small molecules that most often activate G-protein coupled receptors and reconfigure circuit activity and composition. In these systems, modulation has been found to occur at every level, from sensory-motor coupling to neuromuscular transmission (Harris-Warrick and Marder 1991). Neuromodulators have complex effects on motor output; they can alter the firing of individual neurons while also modulating muscle properties, neuromuscular transmission, and sensory neuron response to muscle activity (Fort et al. 2004). We investigated this further by recording the motor output produced by the gastric mill rhythm of the lobster STNS under neuromodulator conditions. How is this neuromuscular system as a whole modulated to produce motor flexibility? We hypothesized that these neuromodulators act on individual receptors of component neurons of central pattern generator (CPG)-effector system themselves and at the periphery, coordinately altering muscle contraction by altering all levels of the crustacean neuromuscular system. Application of NRNFLRFamide, RPCH, oxotremorine, and proctolin to the gastric mill 4 (gm4) muscles of the Cancer crab showed that neuromodulators that have been found to have variable, yet significant effects on the activity of the neurons of the STNS directly alter the activity of the gm4 muscles as well, suggesting that coordination of peripheral actions and direct neuronal modulation regulates patterned motor output.

Date: 2014-05-01

Creator: Lauren A Skerritt

Access: Open access

In the American lobster (Homarus americanus), neurogenic stimulation of the heart drives fluxes of calcium (Ca2+) into the cytoplasm of a muscle cell resulting in heart muscle contraction. The heartbeat is completed by the active transport of calcium out of the cytoplasm into extracellular and intracellular spaces. An increase in the frequency of calcium release is expected to increase amplitude and duration of muscle contraction. This makes sense because an increase in cytoplasmic calcium should increase the activation of the muscle contractile elements (actin and myosin). Since calcium cycling is a reaction-diffusion process, the extent to which calcium mediates contraction amplitude and frequency will depend on the specific diffusion relationships of calcium in this system. Despite the importance of understanding this relationship, it is difficult to obtain experimental information on the dynamics of cytoplasmic calcium. Thus, we developed a mathematical diffusion model of the myofibril (muscle cell) to simulate calcium cycling in the lobster cardiac muscle cell. The amplitude and duration of the force curves produced by the model empirically mirrored that of the experimental data over a range of calcium diffusion coefficients (1-16), nerve stimulation durations (1/6-1/3 of a contraction period), and frequencies (40-80 Hz). The characteristics that alter the response of the lobster cardiac muscle system are stimulation duration (i.e., burst duration), burst frequency, and the rate of calcium diffusion into the cell’s cytoplasm. For this reason, we developed protocols that allow parameters representing these characteristics in the calcium-force model to be determined from isolated whole muscle experiments on lobster hearts (Phillips et al., 2004). These parameters are used to predict variability in lobster heart muscle function consistent with data recorded in experiments. Within the physiological range of nerve stimulation parameters (burst duration and cycle period), calcium increased the cell’s force output for increased burst duration. For example, increased duration of stimulation increased the muscle contraction period and vice versa. In terms of diffusion, a slower rate of calcium diffusion out of the sarcoplasmic reticulum decreased both the calcium level and the contraction duration of the cell. Finally, changes in stimulation frequency did not produce changes in contraction amplitude and duration. When considered in conjunction with experimental stimulations using lobster heart muscle cells, these data illustrate the prominent role for calcium diffusion in governing contraction-relaxation cycles in lobster hearts.