Abstract
The convulsant drug pentylenetetrazol (PTZ) induces tonic depolarization in the identified B1 neuron of Lymnaea stagnalis. Another identified neuron, right parietal dorsal 1 (RPD1), gives the opposite response: tonic hyperpolarization and cessation of spontaneous firing. These effects are mimicked by intracellular injection of calcium ions and reversed following injection of ethylene glycol-bis(β-aminoethyl ether) N, N, N,′ N′-tetraacetic acid (EGTA). Responses to PTZ are retained in the presence of extracellular cobalt ions to block calcium influx. Under voltage clamp, PTZ or injection of calcium ions induces a slow inward current in B1, which is abolished in zero sodium saline. In RPD1 the current response to PTZ or intracellular calcium ions is outward, and is blocked by potassium channel blockers. Thus, differential responses of the two neurons to PTZ appear to be mediated via increased intracellular calcium ions, leading to activation of specific ion currents in each cell type.
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