Clustering through postinhibitory rebound in synaptically coupled neurons

• Published in: Physical review. E, Statistical, nonlinear, and soft matter physics Vol. 70; no. 1 Pt 1; p. 011908
• Main Authors: Chik, D T W, Coombes, S, Wang, Z D
• Format: Journal Article
• Language: English
• Published: United States 01-07-2004
• Subjects: Action Potentials - physiology; Adaptation, Physiological - physiology; Animals; Biological Clocks - physiology; Brain - physiology; Cluster Analysis; Computer Simulation; Differential Threshold - physiology; Humans; Membrane Potentials - physiology; Models, Neurological; Nerve Net - physiology; Neural Inhibition - physiology; Neurons - physiology; Stochastic Processes; Synaptic Transmission - physiology
• ISSN: 1539-3755; 1550-2376
• DOI: 10.1103/PhysRevE.70.011908

Postinhibitory rebound is a nonlinear phenomenon present in a variety of nerve cells. Following a period of hyperpolarization this effect allows a neuron to fire a spike or packet of spikes before returning to rest. It is an important mechanism underlying central pattern generation for heartbeat, swimming and other motor patterns in many neuronal systems. In this paper we consider how networks of neurons, which do not intrinsically oscillate, may make use of inhibitory synaptic connections to generate large scale coherent rhythms in the form of cluster states. We distinguish between two cases (i) where the rebound mechanism is due to anode break excitation and (ii) where rebound is due to a slow T-type calcium current. In the former case we use a geometric analysis of a McKean-type model to obtain expressions for the number of clusters in terms of the speed and strength of synaptic coupling. Results are found to be in good qualitative agreement with numerical simulations of the more detailed Hodgkin-Huxley model. In the second case we consider a particular firing rate model of a neuron with a slow calcium current that admits to an exact analysis. Once again existence regions for cluster states are explicitly calculated. Both mechanisms are shown to prefer globally synchronous states for slow synapses as long as the strength of coupling is sufficiently large. With a decrease in the duration of synaptic inhibition both systems are found to break into clusters. A major difference between the two mechanisms for cluster generation is that anode break excitation can support clusters with several groups, while slow T-type calcium currents predominantly give rise to clusters of just two (antisynchronous) populations.