"... Using a combination of electrophysiological, molecular, and computational approaches, the studies reported here show that D2 dopamine receptor modulation of Na+ currents underlying autonomous spiking contributes to a slowing of discharge rate, such as that seen in vivo. Four lines of evidence support this conclusion. ... Fourth, simulation of cholinergic interneuron pacemaking revealed that a modest increase in the entry of Na+ channels into the slow-inactivated state was sufficient to account for the slowing of pacemaker discharge. These studies establish a cellular mechanism linking dopamine and the reduction in striatal cholinergic interneuron activity seen in the initial stages of associative learning." See paper for more and details.
Model Type: Neuron or other electrically excitable cell
Cell Type(s): Neostriatum interneuron ACh cell
Currents: I Na,t; I K; I h; I K,Ca; I Sodium; I Calcium; I Potassium
Receptors: D2
Model Concept(s): Activity Patterns; Action Potentials; Parkinson's
Simulation Environment: NEURON
Implementer(s): Held, Joshua [j-held at northwestern.edu]
References:
Maurice N et al. (2004). D2 dopamine receptor-mediated modulation of voltage-dependent Na+ channels reduces autonomous activity in striatal cholinergic interneurons. The Journal of neuroscience : the official journal of the Society for Neuroscience. 24 [PubMed]