The role of Ca 2+-dependent cationic current in generating gamma frequency rhythmic bursts: modeling study

Abstract

Fast rhythmic bursting pyramidal neuron or chattering neuron is a promising candidate for the pacemaker of coherent gamma-band (25–70 Hz) cortical oscillation. It, however, still remains to be clarified how the neuron generates such high-frequency bursts. Here, we demonstrate in a single-compartment model neuron that the fast rhythmic bursts (FRBs) can be achieved through Ca 2+-activated channels in the entire gamma frequency range. In a previous in vitro study, a subset of rat cortical pyramidal cells displayed a long-lasting depolarizing afterpotential (DAP) following a plateau-type action potential when K + conductances were suppressed with Cs +, and this DAP was found to be mediated by a Ca 2+-dependent cationic current. This current appeared also suitable for producing a hump-like DAP, a characteristic of the chattering neurons, because of its reversal potential being approximately −40 mV. In the present theoretical study, we show that the enhancement of such a DAP leads to generation of doublet/triplet spikes seen during FRBs. The firing pattern during FRBs is primarily determined by a Ca 2+-dependent cationic current and a small-conductance Ca 2+-dependent potassium current, which are differentially activated by a biphasically decaying Ca 2+ transient produced by fast buffering and a slow pump extrusion after each spike. With varying intensities of injected current pulses, the interburst frequencies of the FRBs range over the entire gamma frequency band (25–70 Hz) in our model, while the intraburst frequencies remain higher than 300 Hz. Our model suggests that FRBs are essentially generated in the soma, unlike the model based on a persistent sodium current, and that the alteration of Ca 2+ sensitivity of Ca 2+-dependent cationic current plays an essential role in controlling the FRB pattern.