Abstract
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.
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