The role of Ca2+-dependent cationic current in generating gamma frequency rhythmic bursts: modeling study.
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 Ca2+-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 Ca2+-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 Ca2+-dependent cationic current and a small-conductance Ca2+-dependent potassium current, which are differentially activated by a biphasically decaying Ca2+ 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 Ca2+ sensitivity of Ca2+-dependent cationic current plays an essential role in controlling the FRB pattern.
Aoyagi
T
T
Department of Applied Analysis and Complex Dynamical Systems, Kyoto University, Sakyoku, 606-8501, Kyoto, Japan.
Kang
Y
Y
Terada
N
N
Kaneko
T
T
Fukai
T
T
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D001683:Biological Clocks / Q000187:drug effects / Q000502:physiology*; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology*; D027682:Cation Transport Proteins / Q000187:drug effects / Q000502:physiology*; D002540:Cerebral Cortex / Q000187:drug effects / Q000502:physiology*; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology*; D008959:Models, Neurological; D010507:Periodicity; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology; D017966:Pyramidal Cells / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology
D027682:Cation Transport Proteins; D007473:Ion Channels; D015221:Potassium Channels; D015222:Sodium Channels; D011188:Potassium