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Ionic Mechanisms Underlying Spontaneous CA1 Neuronal Firing in Ca²⁺-Free Solution

Neural Engineering Center, Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio 44106

Correspondence: Address reprint requests to Dominique M. Durand, Neural Engineering Center, Dept. of Biomedical Engineering, Case Western Reserve University, Cleveland, OH 44106. Tel.: 216-368-3974; Fax: 216-368-4872; E-mail: dxd6{at}po.cwru.edu.

Hippocampal CA1 neurons exposed to zero-[Ca²⁺] solutions can generate periodic spontaneous synchronized activity in the absence of synaptic function. Experiments using hippocampal slices showed that, after exposure to zero-[Ca²⁺]₀ solution, CA1 pyramidal cells depolarized 5–10 mV and started firing spontaneous action potentials. Spontaneous single neuron activity appeared in singlets or was grouped into bursts of two or three action potentials. A 16-compartment, 23-variable cable model of a CA1 pyramidal neuron was developed to study mechanisms of spontaneous neuronal bursting in a calcium-free extracellular solution. In the model, five active currents (a fast sodium current, a persistent sodium current, an A-type transient potassium current, a delayed rectifier potassium current, and a muscarinic potassium current) are included in the somatic compartment. The model simulates the spontaneous bursting behavior of neurons in calcium-free solutions. The mechanisms underlying several aspects of bursting are studied, including the generation of triplet bursts, spike duration, burst termination, after-depolarization behavior, and the prolonged inactive period between bursts. We show that the small persistent sodium current can play a key role in spontaneous CA1 activity in zero-calcium solutions. In particular, it is necessary for the generation of an after-depolarizing potential and prolongs both individual bursts and the interburst interval.

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