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Epileptiform discharges were induced by a reduction of the extracellular Mg<jats:sup>2+<\/jats:sup>concentration to 0.2 mM. These experiments revealed that low concentrations of dopamine (&lt;0.3 \u03bcM) attenuated epileptiform activity, whereas &gt;3 \u03bcM dopamine enhanced epileptiform activity. The D1\u2010agonist SKF38393 (10 \u03bcM) had a strong proconvulsive effect, and the D2\u2010like agonist quinpirole (10 \u03bcM) mediated a weak anticonvulsive effect. The proconvulsive effect of 10 \u03bcM dopamine was completely abolished by the D1\u2010like receptor antagonist SCH39166 (2 \u03bcM) or the D2\u2010like antagonist sulpiride (10 \u03bcM), whereas the D2 antagonist L\u2010741626 (50 nM) and the D3 antagonist SB\u2010277011\u2010A (0.1 \u03bcM) were without effect. The anticonvulsive effect of 0.1 \u03bcM dopamine could be suppressed by D1\u2010like, D2, or D3 receptor antagonists. A proconvulsive effect of 10 \u03bcM dopamine was also observed when AMPA, NMDA, or GABA<jats:sub>A<\/jats:sub>receptors were blocked. In summary, these results suggest that 1) dopamine influences epileptiform activity already at early developmental stages; 2) dopamine can bidirectionally influence the excitability; 3) D1\u2010like receptors mediate the proconvulsive effect of high dopamine concentrations, although the pharmacology of the anticonvulsive effect is less clear; and 4) dopamine\u2010induced alterations in GABAergic and glutamatergic systems may contribute to this effect. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/jnr.23084","type":"journal-article","created":{"date-parts":[[2012,6,20]],"date-time":"2012-06-20T09:28:37Z","timestamp":1340184517000},"page":"2020-2033","source":"Crossref","is-referenced-by-count":6,"title":["Dopaminergic modulation of low\u2010Mg<sup>2+<\/sup>\u2010induced epileptiform activity in the intact hippocampus of the newborn mouse in 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