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Opposite modulation of cortical N-methyl-D-aspartate receptor-mediated responses by low and high concentrations of dopamine.

Abstract：

:To examine whether dopamine modulates cortical N-methyl-D-aspartate receptor-mediated glutamate transmission, whole-cell recordings were made from identified pyramidal cells located in layers V and VI of the medial prefrontal cortex of the rat using a slice preparation. In the presence of tetrodotoxin and the absence of Mg2+, a brief local application of N-methyl-D-aspartate evoked an inward current which was blocked by the N-methyl-D-aspartate antagonist dizocilpine maleate but not affected by the non-N-methyl-D-aspartate antagonist 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline, suggesting that the observed current is mediated by N-methyl-D-aspartate receptors located on recorded cells. Bath application of dopamine produced opposite effects on the N-methyl-D-aspartate current depending on the concentrations of dopamine applied. At low concentrations (<50 microM), dopamine enhanced the N-methyl-D-aspartate current, whereas at higher concentrations, dopamine suppressed the current. The same concentrations of dopamine did not significantly affect the inward current induced by the non-N-methyl-D-aspartate agonist alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid. The enhancing effect of dopamine on the N-methyl-D-aspartate response was mimicked by the D1 agonist SKF38393 and blocked by the D1 antagonist SCH31966, whereas the suppressing effect was mimicked by the D2 agonist quinpirole and blocked by the D2 antagonist eticlopride. The above results suggest that dopamine at low concentrations acts preferentially on D1-like receptors to promote N-methyl-D-aspartate receptor-mediated transmission, while at high concentrations dopamine also activates D2-like receptors, leading to a suppression of the N-methyl-D-aspartate function. This differential modulation of N-methyl-D-aspartate function may have significant implications for understanding behaviors and disorders involving both cortical dopamine- and glutamate-mediated neurotransmission.

journal_name

Neuroscience

journal_title

Neuroscience

authors

Zheng P,Zhang XX,Bunney BS,Shi WX

doi

10.1016/s0306-4522(98)00604-6

keywords:

subject

Has Abstract

pub_date

1999-01-01 00:00:00

pages

527-35

issue

2

eissn

0306-4522

issn

1873-7544

pii

S0306-4522(98)00604-6

journal_volume

91

pub_type

杂志文章

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