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Abstract
The prefrontal cortex is innervated by a well-defined dopaminergic bundle originating
from the brainstem and is a key structure in higher order mental processes. We have
studied the effects of dopamine (DA) on layer V pyramidal cells of the prefrontal
cortex using intracellular recording in rat brain slices maintained in vitro. Bath
administration of DA (50-100 microM) had weak effects on membrane properties of these
neurons. In contrast, DA markedly decreased all components of the synaptic responses
evoked by electrical stimulation of layer I or VI, and in particular the monosynaptic
excitatory postsynaptic potential (EPSP) which arises from activation of glutamatergic
receptors. The afferents from layer VI seemed less affected by DA than those from
layer I. The NMDA (N-methyl-D-aspartate) and AMPA (alpha-amino-3-hydroxy-5-methyl-isoxazolepropionic
acid) components of monosynaptic EPSPs were equally reduced by DA. The isolated fast
gabaergic potential (IPSP) resulting from GABAA receptors activation was similarly
reduced by DA. The suppressive effect of DA on glutamatergic transmission was partially
mimicked by the D1 receptor agonist SKF 38393 (50 microM) whereas the D2 receptor
agonist quinpirole (50 microM) was ineffective. Conversely, this effect was antagonized
by the D1 receptor blocker SCH 23390 (100 microM) but not by the D2 receptor antagonist
sulpiride (100 microM). These findings indicate that DA decreases both glutamatergic
and gabaergic synaptic transmission in neurons located in layer V of rat prefrontal
cortex. These results also suggest that D1 dopamine receptor is involved in the decrement
of glutamatergic transmission. These interactions between DA and glutamate are important
in regard to the suspected implications of both neurotransmitters in psychiatric diseases.