The GABA(B)-mediated modulation of spinal neurons in the lamprey is investigated in this study. Activation of GABA(B) receptors reduces calcium currents through both low- (LVA) and high-voltage activated (HVA) calcium channels, which subsequently results in the reduction of the calcium- dependent potassium (K(Ca)) current. This in turn will reduce the peak amplitude of the afterhyperpolarization (AHP). We used the modulatory effects of GABA(B) receptor activation on N-methyl-D-aspartate (NMDA)-induced, TTX- resistant membrane potential oscillations as an experimental model in which to separate the effects of GABA(B) receptor activation on LVA calcium channels from that on K(Ca) channels. We show experimentally and by using simulations that a direct effect on LVA calcium channels can account for the effects of GABA(B) receptor activation on intrinsic membrane potential oscillations to a larger extent than indirect effects mediated via K(Ca) channels. Furthermore, by conducting experiments and simulations on intrinsic membrane potential oscillations, we find that K(Ca) channels may be activated by calcium entering through LVA calcium channels, providing that the decay kinetics of the calcium that enters through LVA calcium channels is not as slow as the calcium entering via NMDA receptors. A combined experimental and computational analysis revealed that the LVA calcium current also contributes to neuronal firing properties.
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