Abstract
The central motor pattern for heartbeat in the medicinal leech is based upon the alternating bursting activity of mutually inhibitory pairs of heart interneurons (HNs). When pharmacologically isolated, these neurons spike tonically. Using a canonical model of an HN cell (Nadim et al., J. Comput. Neurosci. 2 (1995) 215–235) as a starting point, we generated three models, possessing different subsets of the currents exhibited by HN cells, that are capable of autonomous bursting behavior. These three models represent three different experimentally testable mechanisms that make HN cells potentially capable of bursting or generating slow oscillations under different ionic and pharmacological conditions. The three different mechanisms for producing bursting involve the interplay of: (1)fast Na+ current, leakage current and outward currents, (2)rapidly inactivating low-threshold Ca2+ current, leakage current and outward currents, and (3)slowly inactivating low-threshold Ca2+ current, leakage current and outward currents.
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