RESUMEN
First return maps of interspike intervals for biological neurons that generate repetitive bursts of impulses can display stereotyped structures (neuronal signatures). Such structures have been linked to the possibility of multicoding and multifunctionality in neural networks that produce and control rhythmical motor patterns. In some cases, isolating the neurons from their synaptic network reveals irregular, complex signatures that have been regarded as evidence of intrinsic, chaotic behavior. We show that incorporation of dynamical noise into minimal neuron models of square-wave bursting (either conductance-based or abstract) produces signatures akin to those observed in biological examples, without the need for fine tuning of parameters or ad hoc constructions for inducing chaotic activity. The form of the stochastic term is not strongly constrained and can approximate several possible sources of noise, e.g., random channel gating or synaptic bombardment. The cornerstone of this signature generation mechanism is the rich, transient, but deterministic dynamics inherent in the square-wave (saddle-node and homoclinic) mode of neuronal bursting. We show that noise causes the dynamics to populate a complex transient scaffolding or skeleton in state space, even for models that (without added noise) generate only periodic activity (whether in bursting or tonic spiking mode).
Asunto(s)
Potenciales de Acción/fisiología , Modelos Neurológicos , Neuronas/fisiología , Animales , Simulación por Computador , Ganglios de Invertebrados/fisiología , Dinámicas no Lineales , Palinuridae , Procesos Estocásticos , Transmisión SinápticaRESUMEN
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.
Asunto(s)
Modelos Neurológicos , Neuronas/fisiología , Ruido , Periodicidad , Canales de Sodio/fisiología , Potenciales de Acción/fisiología , Animales , Electrofisiología , Dinámicas no Lineales , Procesos EstocásticosRESUMEN
Using the dynamic clamp technique, we investigated the effects of varying the time constant of mutual synaptic inhibition on the synchronization of bursting biological neurons. For this purpose, we constructed artificial half-center circuits by inserting simulated reciprocal inhibitory synapses between identified neurons of the pyloric circuit in the lobster stomatogastric ganglion. With natural synaptic interactions blocked (but modulatory inputs retained), these neurons generated independent, repetitive bursts of spikes with cycle period durations of approximately 1 s. After coupling the neurons with simulated reciprocal inhibition, we selectively varied the time constant governing the rate of synaptic activation and deactivation. At time constants