  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.
