Gap Junction Effects On Precision And Frequency Of A Model Pacemaker Network. Katherine T. Moortgat1,2, Theodore H. Bullock3,4 and Terrence J. Sejnowski1,5. 1Howard Hughes Medical Institute, Computational Neurobiology Laboratory, The Salk Institute, 10010 North Torrey Pines Road, La Jolla, CA 92037; 2Department of Physics, University of California, San Diego, La Jolla, CA 92093-0354; 3Neurobiology Unit, Scripps Institution of Oceanography, University of CA, San Diego, La Jolla, CA 92093-0201; 4Department of Neuroscience, University of California, San Diego, La Jolla, CA 92093-0354; and 5Department of Biology, University of California, San Diego, La Jolla, CA 92093-0357.
APStracts 6:0499N, 1999.
We investigated the precision of spike timing in a model of gap junction-coupled oscillatory neurons. The model incorporated the known physiology, including the morphology and connectivity, of the weakly electric fish's high frequency and extremely precise pacemaker nucleus (Pn). Two neuron classes, pacemaker and relay cells, were each modeled with two compartments containing Hodgkin-Huxley sodium and potassium currents. Isolated pacemaker cells fired periodically, due to a constant current injection; relay cells were silent but slightly depolarized at rest. When coupled by gap junctions to other neurons, a model neuron, like its biological correlate, spiked at frequencies and amplitudes that were largely independent of current injections. The phase distribution in the network was labile to intracellular current injections and to gap junction conductance changes. The model predicts a biologically plausible gap junction conductance of 4 5 nanoSiemens (200 250 M). This results in a coupling coefficient of approximately 0.02, as observed in vitro. Network parameters were varied to test which could improve the temporal precision of oscillations. Increased gap junction conductances and larger numbers of cells (holding total junctional conductance per cell constant) both substantially reduced the coefficient of variation (CV=standard deviation=mean) of relay cell spike times by 74 85% and more; and did so with lower gap junction conductance when cells were contacted axonically compared to somatically. Pacemaker cell CV was only reduced when the probability of contact was increased, and then only moderately: a five-fold increase in the probability of contact reduced CV by 35%. We conclude that gap junctions facilitate synchronization, can reduce CV, are most effective between axons, and that pacemaker cells must have low intrinsic CV to account for the low CV of cells in the biological network.
Received 4 March 1999; accepted in final form 5 October 1999.
APS Manuscript Number J237-9.
Article publication pending Journal of Neurophysiology.
ISSN 1080-4757 Copyright 1999 The American Physiological Society.
Published in APStracts on 21 December 1999