A Physiologically Plausible Model of Action Selection and Oscillatory Activity in the Basal Ganglia

Abstract

The basal ganglia (BG) have long been implicated in both motor function and dysfunction. It has been proposed that the BG form a centralized action selection circuit, resolving conflict between multiple neural systems competing for access to the final common motor pathway. We present a new spiking neuron model of the BG circuitry to test this proposal, incorporating all major features and many physiologically plausible details. We include the following: effects of dopamine in the subthalamic nucleus (STN) and globus pallidus (GP), transmission delays between neurons, and specific distributions of synaptic inputs over dendrites. All main parameters were derived from experimental studies. We find that the BG circuitry supports motor program selection and switching, which deteriorates under dopamine-depleted and dopamine-excessive conditions in a manner consistent with some pathologies associated with those dopamine states. We also validated the model against data describing oscillatory properties of BG. We find that the same model displayed detailed features of both ␥-band

Conditions for the Generation of Beta Oscillations in the Subthalamic Nucleus–Globus Pallidus Network

“…Relationship to other models There have been a number of other modeling studies that investigated the oscillations present in the basal ganglia (Gillies et al, 2002;Terman et al, 2002;Humphries et al, 2006;Leblois et al, 2006). Two of those studies (Gillies et al, 2002;) also focused on the STN-GPe circuit and found that it can generate oscillatory activity, but the mechanisms that generated these oscillations were very different from our model, as we now describe.…”

“…Two other models simulated a more general circuit including the cortex, the basal ganglia, and the thalamus (Humphries et al, 2006;Leblois et al, 2006). Leblois et al (2006) observed oscillatory behavior in theta-alpha band for realistic values of transmission delays.…”

“…Similar changes in STN-GPe synaptic weights to model dopamine depletion have been used in a previous computational model (Humphries et al, 2006).…”

“…To shed light on the origin of oscillations associated with Parkinson's disease, many computational models have been proposed (Gillies et al, 2002;Terman et al, 2002;Frank, 2006;Humphries et al, 2006;Leblois et al, 2006;Gillies and Willshaw, 2007;van Albada and Robinson, 2009). These models provide interesting conclusions and explain experimentally observed phenomena; however, most have a drawback in that the complexity of the equations used in the model make them unsuitable for mathematical analysis.…”

Dopamine-modulated dynamic cell assemblies generated by the GABAergic striatal microcircuit

“…While an interesting hypothesis, this mapping does not account for the microcircuit of the striatum, or the effects of the numerous neuromodulators within it. Other models of the whole basal ganglia circuit do not rely on the local collaterals within striatum for their computations, rather proposing that the striatum is both integrator of diverse cortical information and filter on weak cortical inputs, as the first stage of an input selection mechanism implemented by the whole basal ganglia (as opposed to just the striatum), (Gurney et al, 2001;Humphries et al, 2006) -but these models too do not account for the striatal microcircuit.…”