Motor organization of Tritonia swimming. III. Contribution of intrinsic membrane properties to flexion neuron burst formation.

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Abstract
During escape swimming in Tritonia, flexion neurons in the pedal ganglia produce recurrent bursts of activity that differ dramatically from cell to cell. The form of the bursts in each identified cell is highly stereotyped from swim to swim and from animal to animal. The role of intrinsic membrane properties in forming the cell-specific bursts is studied. All flexion neurons studied possessed the intrinsic property of spike frequency adaptation to maintained excitation. The magnitude of this adaptation was more pronounced in 1 class of flexion neurons (DFN-A) than in 3 other classes (DFN-B, VFN, class III). Spike frequency adaptation in the DFN-A was mediated predominantly by a Ca-activated K current, since adaptation was almost completely blocked by replacing external Ca with the Ca channel blockers Co or Mn, and adaptation was always associated with a postburst hyperpolarization that had a reversal potential that was sensitive to the external K concentration. The role of spike frequency adaptation in shaping swim bursts was assessed by intracellular injection of the Ca chelator EGTA (ethylene glycol-bis(.beta.-aminoethyl ether)-N,N''-tetraacetic acid), which largely blocks spike frequency adaptation. The swim bursts of DFN-A were dramatically altered after EGTA injection; in other cells (DFN-B, VFN, class III) EGTA injection had little or no effect. The form of the synaptic drive and intrinsic membrane properties appear to be important in determining flexion neuron bursts. The DFN-A bursts are formed by the interaction between synaptic and intrinsic properties; bursts in the DFN-B, VFN and class III cells are formed predominantly by their synaptic drive.