Journal of Computational Neuroscience

, Volume 21, Issue 3, pp 307-328

Differential control of active and silent phases in relaxation models of neuronal rhythms

  • Joël TabakAffiliated withLaboratory of Neural Control, NINDS/NIHDepartment of Biological Science, Florida State University Email author 
  • , Michael J. O'DonovanAffiliated withLaboratory of Neural Control, NINDS/NIH
  • , John RinzelAffiliated withCenter for Neural Science and Courant Institute of Mathematical Sciences, New York University

Rent the article at a discount

Rent now

* Final gross prices may vary according to local VAT.

Get Access


Rhythmic bursting activity, found in many biological systems, serves a variety of important functions. Such activity is composed of episodes, or bursts (the active phase, AP) that are separated by quiescent periods (the silent phase, SP). Here, we use mean field, firing rate models of excitatory neural network activity to study how AP and SP durations depend on two critical network parameters that control network connectivity and cellular excitability. In these models, the AP and SP correspond to the network's underlying bistability on a fast time scale due to rapid recurrent excitatory connectivity. Activity switches between the AP and SP because of two types of slow negative feedback: synaptic depression—which has a divisive effect on the network input/output function, or cellular adaptation—a subtractive effect on the input/output function. We show that if a model incorporates the divisive process (regardless of the presence of the subtractive process), then increasing cellular excitability will speed up the activity, mostly by decreasing the silent phase. Reciprocally, if the subtractive process is present, increasing the excitatory connectivity will slow down the activity, mostly by lengthening the active phase. We also show that the model incorporating both slow processes is less sensitive to parameter variations than the models with only one process. Finally, we note that these network models are formally analogous to a type of cellular pacemaker and thus similar results apply to these cellular pacemakers.


Excitatory network Synaptic depression Cellular adaptation Episodic activity Mean field model