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The Journal of Neurophysiology Vol. 84 No. 1 July 2000, pp. 112-119
Copyright ©2000 by the American Physiological Society
1Department of Neurophysiology, Institute of Physiology, University Hospital Charité, Humboldt University Berlin, 10117 Berlin, Germany; and 2Department of Cellular and Molecular Pharmacology, University of California, San Francisco, California 94141-0450
Behr, Joachim,
Tengis Gloveli,
Dietmar Schmitz, and
Uwe Heinemann.
Dopamine Depresses Excitatory Synaptic Transmission Onto Rat
Subicular Neurons Via Presynaptic D1-Like Dopamine Receptors. J. Neurophysiol. 84: 112-119, 2000. Schizophrenia is considered to be associated with an abnormal
functioning of the hippocampal output. The high clinical potency of
antipsychotics that act as antagonists at dopamine (DA) receptors indicate a hyperfunction of the dopaminergic system. The subiculum obtains information from area CA1 and the entorhinal cortex and represents the major output region of the hippocampal complex. To
clarify whether an enhanced dopaminergic activity alters the hippocampal output, the effect of DA on alveus- and perforant path-evoked excitatory postsynaptic currents (EPSCs) in subicular neurons was examined using conventional intracellular and whole cell
voltage-clamp recordings. Dopamine (100 µM) depressed
alveus-elicited (S)-
-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated EPSCs to 56 ± 8% of control while perforant path-evoked EPSCs were attenuated to only 76 ± 7% of control. Dopamine had no effect on the EPSC kinetics. Dopamine reduced the
frequency of spontaneous miniature EPSCs without affecting their
amplitudes. The sensitivity of subicular neurons to the glutamate
receptor agonist (S)--amino-3-hydoxy-5-methyl-4-isoxazolepropionic acid was unchanged by DA pretreatment, excluding a postsynaptic mechanism for the observed reduction of excitatory synaptic
transmission. The effect of DA on evoked EPSCs was mimicked by the D1
receptor agonist SFK 38393 and partially antagonized by the D1 receptor antagonist SCH 23390. While the D2 receptor agonist quinelorane failed
to reduce the EPSCs, the D2 receptor antagonist sulpiride did not block
the action of DA. The results indicate that DA strongly depresses the
hippocampal and the entorhinal excitatory input onto subicular neurons
by decreasing the glutamate release following activation of presynaptic
D1-like DA receptors.
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