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This Article Full Text Full Text (PDF) All Versions of this Article: 568/1/243    most recent jphysiol.2005.091843v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tamae, A. Articles by Yoshimura, M. Search for Related Content PubMed PubMed Citation Articles by Tamae, A. Articles by Yoshimura, M.

¹ Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan
² Department of Physiology, Faculty of Medicine, Saga University, Saga 849-8501, Japan

Dopaminergic innervation of the spinal cord is largely derived from the brain. To understand the cellular mechanisms of antinociception mediated by descending dopaminergic pathways, we examined the actions of dopamine (DA) on nociceptive transmission by using behavioural studies and whole-cell patch-clamp recordings from substantia gelatinosa (SG) neurones in the spinal cord. Intrathecal administration of DA increased the mechanical nociceptive threshold and this effect was mimicked by a D2-like receptor agonist, quinpirole, but not by a D1-like receptor agonist, SKF 38393. In current-clamp mode of patch-clamp recordings, bath application of DA hyperpolarized the membrane potential of SG neurones and suppressed action potentials evoked by electrical stimulation of a dorsal root. In voltage-clamp mode, DA induced an outward current that was resistant to TTX, was blocked by the addition of Cs⁺ or GDP-ß-S in the pipette solution, and was inhibited in the presence of Ba⁺. The DA-induced current reversed its polarity at a potential close to the equilibrium potential of the K⁺ channel calculated from the Nernst equation. The DA-induced outward current was mimicked by quinpirole, but not by SKF 38393. The DA-induced outward current was suppressed by a D2-like receptor antagonist, sulpiride, but not by a D1-like receptor antagonist, SCH 23390. In contrast, DA did not cause any significant change in amplitude and frequency of miniature excitatory postsynaptic currents (mEPSCs). These results indicate that DA mainly acts on postsynaptic SG neurones to induce an outward current via G-protein-mediated activation of K⁺ channels through D2-like receptors. This may be a possible mechanism for antinociception by the descending dopaminergic pathway.

(Received 1 June 2005; accepted after revision 16 June 2005; first published online 23 June 2005)
Corresponding author T. Nakatsuka: Department of Physiology, Faculty of Medicine, Saga University, Saga 849-8501, Japan. Email: nakatsuk{at}cc.saga-u.ac.jp

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