We use a realistic computational model of dopaminergic neurons in vivo to suggest that ethanol, through its effects on Ih, modifies the temporal structure of the spiking activity. The model predicts that the dopamine level may increase much more during bursting than pacemaking activity, especially in those brain regions with a slow dopamine clearance rate. The results suggest that a selective pharmacological remedy could thus be devised against the rewarding effects of ethanol that are postulated to mediate alcohol abuse and addiction, targeting the specific HCN genes expressed in dopaminergic neurons.
Cell Type(s): Substantia nigra pars compacta DA cell
Simulation Environment: NEURON
Implementer(s): Migliore, Michele [Michele.Migliore at Yale.edu]
Migliore M, Cannia C, Canavier CC. (2008). A modeling study suggesting a possible pharmacological target to mitigate the effects of ethanol on reward-related dopaminergic signaling. Journal of neurophysiology. 99 [PubMed]