Fig. 4: DA actions at D1R have an inverted U dose response on dlPFC Delay cell firing. | Neuropsychopharmacology

Fig. 4: DA actions at D1R have an inverted U dose response on dlPFC Delay cell firing.

From: Neuromodulation of prefrontal cortex cognitive function in primates: the powerful roles of monoamines and acetylcholine

Fig. 4: DA actions at D1R have an inverted U dose response on dlPFC Delay cell firing.

A With insufficient DA stimulation of D1R, there is inadequate Delay cell firing (A1). It is hypothesized that D1R-cAMP-PKA actions are needed to phosphorylate NMDAR and maintain them within the synapse. B Under optimal conditions, moderate levels of D1R-cAMP-PKA activity phosphorylate NMDAR to maintain them in the postsynaptic density (PSD) and promote calcium entry through NMDAR. Moderate levels of internal calcium release would also support neurotransmission, and enhance delay-related firing (B1). C High levels of D1R-cAMP-PKA actions, e.g., as occurs during uncontrollable stress, cause a loss of Delay cell firing (C1) by opening large numbers of nearby K+ channels. Note that more subtle increases can selectively gate out “noise,” i.e., inputs from nonpreferred directions, enhancing neuronal tuning. This can be seen in Fig. 6.

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