We report experimental studies of synchronization phenomena in a pair of biological neurons that interact through naturally occurring, electrical coupling. When these neurons generate irregular bursts of spikes, the natural coupling synchronizes slow oscillations of membrane potential, but not the fast spikes. By adding artificial electrical coupling we studied transitions between synchrony and asynchrony in both slow oscillations and fast spikes. We discuss the dynamics of bursting and synchronization in living neurons with distributed functional morphology.Comment: 4 pages, 6 figures, to be published in PR

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Chaotic bursting has been recorded in synaptically isolated neurons of the pyloric central pattern generating (CPG) circuit in the lobster stomatogastric ganglion. Conductance-based models of pyloric neurons typically fail to reproduce the observed irregular behavior in either voltage time series or state-space trajectories. Recent suggestions of Chay [Biol Cybern 75: 419-431] indicate that chaotic bursting patterns can be generated by model neurons that couple membrane currents to the nonlinear dynamics of intracellular calcium storage and release. Accordingly, we have built a two-compartment model of a pyloric CPG neuron incorporating previously described membrane conductances together with intracellular Ca2+ dynamics involving the endoplasmic reticulum and the inositol 1,4,5-trisphosphate receptor IP3R. As judged by qualitative inspection and quantitative, nonlinear analysis, the irregular voltage oscillations of the model neuron resemble those seen in the biological neurons. Chaotic bursting arises from the interaction of fast membrane voltage dynamics with slower intracellular Ca2+ dynamics and, hence, depends on the concentration of IP3. Despite the presence of 12 independent dynamical variables, the model neuron bursts chaotically in a subspace characterized by 3-4 active degrees of freedom. The critical aspect of this model is that chaotic oscillations arise when membrane voltage processes are coupled to another slow dynamic. Here we suggest this slow dynamic to be intracellular Ca2+ handling.

We explore the effects of stochastic sodium (Na) channel activation on the variability and dynamics of spiking and bursting in a model neuron. The complete model segregates Hodgin-Huxley-type currents into two compartments, and undergoes applied current-dependent bifurcations between regimes of periodic bursting, chaotic bursting, and tonic spiking. Noise is added to simulate variable, finite sizes of the population of Na channels in the fast spiking compartment. During tonic firing, Na channel noise causes variability in interspike intervals (ISIs). The variance, as well as the sensitivity to noise, depend on the model's biophysical complexity. They are smallest in an isolated spiking compartment; increase significantly upon coupling to a passive compartment; and increase again when the second compartment also includes slow-acting currents. In this full model, sufficient noise can convert tonic firing into bursting. During bursting, the actions of Na channel noise are state-dependent. The higher the noise level, the greater the jitter in spike timing within bursts. The noise makes the burst durations of periodic regimes variable, while decreasing burst length duration and variance in a chaotic regime. Na channel noise blurs the sharp transitions of spike time and burst length seen at the bifurcations of the noise-free model. Close to such a bifurcation, the burst behaviors of previously periodic and chaotic regimes become essentially indistinguishable. We discuss biophysical mechanisms, dynamical interpretations and physiological implications. We suggest that noise associated with finite populations of Na channels could evoke very different effects on the intrinsic variability of spiking and bursting discharges, depending on a biological neuron's complexity and applied current-dependent state. We find that simulated channel noise in the model neuron qualitatively replicates the observed variability in burst length and interburst interval in an isolated biological bursting neuron.