A model of dopamine modulated cortical activation.
Standard techniques from pharmacology and current theories on the biochemistry of dopamine (DA) are used to derive a new model of how DA modulates cortical activation. The model assumes that DA potentiates the glutamate response through the NMDA receptor and depresses the glutamate response through non-NMDA receptors. A static version of the model is used to examine the neurobiological plausibility of the Servan-Schreiber, Printz, and Cohen model [Science 249 (1990) 892]. A dynamic version can be used to model many behaviors that are outside the domain of the static [Science 249 (1990) 892] model, including single-cell recording data. As a preliminary test of the model, we show that it can account for some single-cell recording data that examined the effects of DA on the firing rate of glutamatergic cortical cells.
Ashby
F Gregory
FG
Department of Psychology, University of California at Santa Barbara, Santa Barbara, CA 93106, USA. ashby@psych.ucsb.edu
Casale
Michael B
MB
D002540:Cerebral Cortex / Q000502:physiology*; D004298:Dopamine / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D018091:Receptors, AMPA / Q000502:physiology; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology
D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; D004298:Dopamine