High level modeling of tonic dopamine mechanisms in striatal neurons

Abstract

The extant versions of many basal ganglia models use a `gating' model of dopamine function which enhances input to D1 receptor units and attenuates input to D2 receptor units. There is evidence that this model is unsatisfactory because (a) there are not sufficient dopaminergic synapses to gate all input and (b) dopamine's main effect is likely to be on the ion-channels contributing to the neuron's membrane potential. Thus, an alternative output function-based model of dopamine's effect is proposed which accounts for the dopamine-mediated changes in ion-channel based currents. Simulation results show that the selection and switching properties of the intrinsic and extended models are retained with the new models. The parameter regimes under which this occurs leads us to predict that an L-type Ca2+ current is likely to be the major determinant of striatal neuron output if the basal ganglia is indeed an action selection mechanism. In addition, the results provide evidence that increasing dopamine can improve a neuron's signal-to-noise ratio.