This paper introduces a new approach to the modeling of capacitance in field-effect transistor (FET) devices, which we call division by current. It is compared with existing formulations, which we call division by capacitance and division by charge. In doing so, it is necessary to normalize the theory of nonlinear capacitances and to clarify a number of matters. These include charge conservation and determination of charge functions from capacitance measurements, which are often misstated in the literature. We find the division by current formulation to be practical and to have significant advantages in the generation of FET models and in circuit simulation.

Transmitter release in neurons is triggered by intracellular Ca2+ increase via the opening of voltage-gated Ca2+ channels. Here we investigated the voltage-gated Ca2+ channels in wide-field amacrine cells (WFACs) isolated from the white-bass retina that are functionally coupled to transmitter release. We monitored transmitter release through the measurement of the membrane capacitance (Cm). We found that 500-ms long depolarizations of WFACs from −70 mV to 0 mV elicited about a 6% transient increase in the Cm or membrane surface area. This Cm jump could be eliminated either by intracellular perfusion with 10 mM BAPTA or by extracellular application of 4 mM cobalt. WFACs possess N-type and L-type voltage-gated Ca2+ channels. Depolarization-evoked Cm increases were unaffected by the specific N-type channel blocker ω-conotoxin GVIA, but they were markedly reduced by the L-type blocker diltiazem, suggesting a role for the L-type channel in synaptic transmission. Further supporting this notion, in WFACs the synaptic protein syntaxin always colocalized with the pore-forming subunit of the retinal specific L-type channels (CaV1.4 or α1F), but never with that of the N-type channels (CaV2.2 or α1B).