MODELING SLOWLY BURSTING NEURONS VIA CALCIUM STORE AND VOLTAGE-INDEPENDENT CALCIUM CURRENT

Recent experiments indicate that the calcium store (e.g., endoplasmic reticulum) is involved in electrical bursting and [Ca2+](i) oscillatio n in bursting neuronal cells. In this paper, we formulate a mathematic al model for bursting neurons, which includes Ca2+ in the intracellula r Ca2+ stores and a voltage-independent calcium channel (VICC). This V ICC is activated by a depletion of Ca2+ concentration in the store, [C a2+](CS). In this model, [Ca2+](CS) oscillates slowly, and this slow d ynamic in turn gives rise to electrical bursting. The newly formulated model thus is radically different from existing models of bursting ex citable cells, whose mechanism owes its origin to the ion channels in the plasma membrane and the [Ca2+](i) dynamics. In addition, this mode l is capable of providing answers to some puzzling phenomena, which th e previous models could not (e.g., why cAMP, glucagon, and caffeine ha ve ability to change the burst periodicity). rising mag-fura-2 fluores cent dyes, it would be interesting to verify the prediction of the mod el that (1) [Ca2+](CS) oscillates in bursting neurons such as Aplysia neuron and (2) the neurotransmitters and hormones that affect the aden ylate cyclase pathway can influence this oscillation.