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* Howard Hughes Medical Institute and Molecular and Computational
Neurobiology Laboratory, The Salk Institute, 10010 North Torrey Pines
Road, La Jolla, CA 92037; Contributed by Charles F. Stevens, October 30, 2000
Dopamine acts mainly through the D1/D5 receptor in the prefrontal
cortex (PFC) to modulate neural activity and behaviors associated with
working memory. To understand the mechanism of this effect, we examined
the modulation of excitatory synaptic inputs onto layer V PFC pyramidal
neurons by D1/D5 receptor stimulation. D1/D5 agonists increased the
size of N-methyl-D-aspartate (NMDA)
component of excitatory postsynaptic currents (EPSCs) through a
postsynaptic mechanism. In contrast, D1/D5 agonists caused a slight
reduction in the size of the non-NMDA component of EPSCs through a
small decrease in release probability. With 20 Hz synaptic trains, we found that the D1/D5 agonists increased depolarization of summating the NMDA component of excitatory postsynaptic potential (EPSP). By
increasing the NMDA component of EPSCs, yet slightly reducing release,
D1/D5 receptor activation selectively enhanced sustained synaptic
inputs and equalized the sizes of EPSPs in a 20-Hz train.
Neurobiology
Dopamine D1/D5 receptor modulation of excitatory synaptic
inputs to layer V prefrontal cortex neurons
,
, Division of Basic Medical
Sciences, University of South Dakota School of Medicine, 414 East Clark
Street, Vermillion, SD 57069; and § Department of
Biology, University of California at San Diego, La Jolla, CA 92093
To whom reprint requests should be addressed. E-mail:
jeremy{at}salk.edu.
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