Date: 2025-01-01

Creator: Yasemin Altug

Access: Open access

In order to maintain circuit stability through environmental perturbations, such as increases in temperature, neural circuits are able to adjust their output via modulatory and ion channel regulation. For instance, peptide modulators enable the lobster cardiac neuromuscular system to sustain physiological function at temperatures that surpass the crash temperature of the organ in the absence of modulation. Crash temperature is defined as the temperature at which neural activity ceases. For a crash, this temperature induced loss of activity is recovered when temperature is returned within the permissible range. Thus, it is hypothesized that there are underlying physiological mechanisms employed by the nervous system that compensates for changes in temperature and provides stability within acute temperature fluctuations. Neuromodulatory mechanisms have been proposed as one hypothesis that provide this temperature compensation. In accordance with previously collected data (Lemus 2022), I hypothesized that myosuppressin, a crustacean neuropeptide, provides stability during acute temperature variations. Because myosuppressin acts on the cardiac neurons and muscles separately, we hypothesized that the myosuppressin-induced increase in heart contraction amplitude, and decrease in contraction period can offset each other to provide system stability as temperature is increased. To test whether or not myosuppressin stabilizes circuit output as temperature is increased, myosuppressin was applied to the lobster whole heart at 7ºC, 10ºC, 13ºC and 16ºC, for 20 minutes. Changes in cardiac output in response to temperature and modulation were assessed by measuring the contraction force, heart beat frequency, and minimum contraction force. Interestingly, and contrary to previous results, in this data set, the cardiac neuromuscular system was temperature compensated in saline alone (control), and was not temperature compensated when perfused with myosuppressin (10-6 M). These findings seemed to differ from Lemus’ data (2023), where the cardiac neuromuscular system was not temperature compensated in control conditions and became temperature compensated when perfused with myosuppressin. The seasons at which each data set was collected (June-August vs November-March) could underlie these observed discrepancies.

Date: 2021-01-01

Creator: Grace Marie Hambelton

Access: Open access

Baroreceptors are stretch receptors located in the aorta of mammals; in response to increased afterload, they elicit a decrease in heart rate, creating a negative feedback loop that lowers blood pressure. Although lobsters (Homarus americanus) do not have baroreceptors like mammals, closely related land crabs have been shown to have baroreceptor-like responses. Heart contraction is also regulated by the Frank-Starling response, where increasing stretch or preload increases the contractile force of the heart. In addition to these types of biomechanical modulations, lobsters use a central pattern generator, the cardiac ganglion, to maintain synchronicity of the heartbeat. The heart is also controlled by the central nervous system via neuromodulators, such as myosuppressin, which has been shown to increase active force and decrease frequency in isolated lobster hearts. We performed experiments on a lobster heart with the main arteries still intact, and varied the preload by stretching anterior arteries, and the afterload by elevating the dorsal abdominal artery. We added myosuppressin to modulate the cardiac ganglion output and muscle contraction. We found that the baroreceptor-like response is most directly modulated by active force, whereas frequency could be a secondary control. Increasing preload does increase active force, but that does not correlate to a higher cardiac output, which shows that how hard the heart pumps is not what determines how effectively it is pumping. Additionally, we found that myosuppressin has a much stronger effect on frequency than active force, and so with myosuppressin, frequency becomes the main determinant of cardiac output.