Elsevier

Neuroscience Letters

Volume 158, Issue 2, 20 August 1993, Pages 217-220
Neuroscience Letters

Evidence for D1 dopamine receptor-mediated modulation of the synaptic transmission from motor axon collaterals to Renshaw cells in the rat spinal cord

https://doi.org/10.1016/0304-3940(93)90268-PGet rights and content

Abstract

The possible modulatory role of D1 dopamine receptors on the excitability of lumbar spinal Renshaw cells was studied in anesthetized rats spinalized at T4 level. Burst responses elicited by single electrical shocks to ipsilateral ventral roots L6 (frequency 0.5 Hz, stimulus width 0.1 ms) and spontaneous activity were recorded extracellularly using conventional 3 M KCl filled glass micropipettes. The specific D1 agonist SKF 38393 (0.5-1 mg/kg i.v.) enhanced Renshaw cell burst responses by 20–60% (n=7) and increased their spontaneous discharge rate (n=3). This effect was clearly antagonized by the specific D1 antagonist SCH 23390 (1 mg/kg i.v.) although SCH 23390 proved ineffective per se. We conclude that SKF 38393 induced facilitation was due to activation of the specific D1 receptors which could be the functional counterpart of the presynaptic D2 receptors described earlier by us in the same synapse.

References (28)

Cited by (13)

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    Our data suggest that over short periods, activation of D1-like receptors increases the open probability and open duration of AMPA channels. Our data provide one mechanism whereby activation of D1 receptors can increase the excitability of spinal motor networks in rats (Seth et al., 1993; Barriere et al., 2004) and mice (Madriaga et al., 2004). In combination with our previous work demonstrating that DA enhances motoneuronal sEPSCs and mEPSCs and enhances puff-evoked AMPA currents (Han et al., 2007), our work strongly suggests that DA's modulation of AMPA channels through D1-like receptors is an important mechanism contributing to motoneuron excitability.

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Present address: Physiologisches Institut, Heinrich-Heine-Universität, Düsseldorf, FRG.

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