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

摘要

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.