
Nematode neurons generally produce graded potentials instead of action potentials. It is unclear how the graded potentials control postsynaptic cells under physiological conditions. Here we show that postsynaptic currents frequently occur in bursts at the neuromuscular junction of Caenorhabditis elegans. Cholinergic bursts concur with facilitated action potential firing, elevated cytosolic [Ca(2+)] and contraction of the muscle whereas GABAergic bursts suppress action potential firing. The bursts, distinct from artificially evoked responses, are characterized by a persistent current (the primary component of burst-associated charge transfer) and increased frequency and mean amplitude of postsynaptic current events. The persistent current of cholinergic postsynaptic current bursts is mostly mediated by levamisole-sensitive acetylcholine receptors, which correlates well with locomotory phenotypes of receptor mutants. Eliminating command interneurons abolishes the bursts whereas mutating SLO-1 K(+) channel, a potent presynaptic inhibitor of exocytosis, greatly increases the mean burst duration. These observations suggest that motoneurons control muscle by producing postsynaptic current bursts.
Muscle Cells, Action Potentials, Synaptic Potentials, Article, Cholinergic Neurons, Optogenetics, Interneurons, Mutation, Synapses, Animals, Large-Conductance Calcium-Activated Potassium Channels, GABAergic Neurons, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Muscle, Skeletal, Evoked Potentials
Muscle Cells, Action Potentials, Synaptic Potentials, Article, Cholinergic Neurons, Optogenetics, Interneurons, Mutation, Synapses, Animals, Large-Conductance Calcium-Activated Potassium Channels, GABAergic Neurons, Caenorhabditis elegans, Caenorhabditis elegans Proteins, Muscle, Skeletal, Evoked Potentials
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