The Effects of Temperature on the Cardiac System of the American Lobster, Homarus americanus
2014
- 2,373Usage
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Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Usage2,373
- Downloads2,158
- 2,158
- Abstract Views215
Artifact Description
The American lobster, Homarus americanus, inhabits a large oceanic range spanning from Labrador, Canada to North Carolina, USA. This geographic range varies in temperature by as much as 25ºC, and daily temperature fluctuations of up to 12ºC may occur at a single location depending on season, water depth, and tides. The cardiac system of the lobster is sensitive to these temperature changes, and has been shown to adjust its functioning over a large temperature range. A previous study showed that various functional parameters respond differently to temperature changes, but a stable cardiac output can be maintained over the range of 2-20ºC. The current study showed that the effects of temperature were exerted primarily through changes in the lobster heart central pattern generator, the cardiac ganglion. Similar patterns of change were seen in both semi-intact hearts and isolated cardiac ganglion preparations in response to increasing temperature. Specifically, with increasing temperature, the burst frequency showed a biphasic pattern in which frequency initially increased, then decreased rapidly at high temperatures. The burst duration, duty cycle, and number of spikes per burst generally decreased with increasing temperature, and spike frequency increased over the entire temperature range. Semi-intact hearts and isolated cardiac ganglia showed similar “crash” patterns, characterized by complete loss of function at high temperatures and complete recovery of function when temperature was returned to baseline. Feedback in the semi-intact heart provided some stabilization of bursting activity, but it did not provide the expected protection from high temperatures. The isolated CG had a significantly higher crash temperature than did the semi-intact system. This discrepancy in crash temperatures may be explained by considering factors at the level of the muscle and neuromuscular junction (NMJ), such as stretch and nitric oxide (NO) feedback and the balance of facilitation and depression at the NMJ. Stimulated preparations showed defacilitation of contraction amplitude at high temperatures despite the maintenance of constant burst parameters of stimulation. Therefore, several factors contributing to the relatively low crash temperature of the intact system may be a shift in the balance of facilitation and depression at the NMJ, a depression in ganglion function due to the release of NO by the muscle, or a combination of the two mechanisms.
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