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The Journal of Neurophysiology Vol. 86 No. 6 December 2001, pp. 2911-2918
Copyright ©2001 by the American Physiological Society
Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294
Gonzalez-Islas, Carlos and
John J. Hablitz.
Dopamine Inhibition of Evoked IPSCs in Rat Prefrontal Cortex. J. Neurophysiol. 86: 2911-2918, 2001. Rat prefrontal cortex (PFC) receives substantial dopamine (DA) input.
This DA innervation appears critical for modulation of PFC cognitive
functions. Clinical and experimental studies have also implicated DA in
the pathogenesis of a number of neurological and psychiatric disorders
including epilepsy and schizophrenia. However, the actions of DA at the
cellular level are incompletely understood. Both inhibitory
interneurons and pyramidal cells are targets of DA and may express
different DA receptor types. Our recent findings suggest that DA can
directly excite cortical interneurons and increase the frequency of
spontaneous inhibitory postsynaptic currents (IPSCs). The present study
was undertaken to determine the effect of specific DA receptor agonists
on evoked (e) IPSCs. Visually identified pyramidal neurons were studied
using whole cell voltage-clamp techniques. Bath application of DA 30 µM reduced IPSC amplitude to 80 ± 4% (mean ± SE) of
control without any significant change in IPSC kinetics or passive
membrane properties. The D1-like DA receptor agonist SKF 38393 reduced
IPSC amplitude to 71.5 ± 8%, whereas the D2-like specific
agonist quinpirole has no effect on amplitude (94.5 ± 5%). The
D1-like receptor antagonist SCH 23390 prevented DA inhibition of IPSC
amplitude (98.2 ± 4%), whereas IPSCs were still reduced in
amplitude (79.7 ± 4%) by DA in the presence of the D2-like
receptor antagonist sulpiride. DA increased significantly paired-pulse
inhibition, whereas responses to puff applied GABA were unaffected.
Addition of the PKA inhibitor H-8 blocked the effect of DA on IPSCs.
These results suggest that DA can decrease IPSCs in layer II-III PFC
neocortical pyramidal cells by activating presynaptic D1-like receptors.
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