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| Research article summary (published 11 Jan 2009): |
Cell-dependent physiological synaptic action of morphine in the rat habenular nucleus: morphine both inhibits and facilitates excitatory synaptic transmission.
Full Abstract
Although several lines of evidence have suggested that the activity of thalamic neurons is modulated by opioids, the mechanism by which morphine in the thalamus regulates the release of excitatory neurotransmitters remains unclear. In the present study, we investigated the synaptic modulation of morphine to regulate excitatory synaptic transmission, probably glutamatergic transmission, in habenular nucleus (Hb) and centrolateral nucleus (CL) neurons in the rat thalamus. Using the whole-cell patch-clamp technique, we found dual modulation by morphine in Hb neurons: morphine caused either inhibition or facilitation of the miniature excitatory postsynaptic current (mEPSC) frequency in the Hb. In Hb neurons that showed a morphine-induced decrease in the mEPSC frequency, the mEPSC amplitude was also decreased in the presence of morphine. In contrast, the mEPSC amplitude was markedly increased in Hb neurons that showed a morphine-induced increase in the mEPSC frequency. We also observed a significant decrease in the mEPSC frequency with morphine in CL neurons without any change in the mEPSC amplitude, whereas morphine did not facilitate the mEPSC frequency in CL neurons. These results suggest that morphine may induce cell-dependent dual modulation of glutamatergic synaptic transmission in the Hb.
Author information
Author/s: Hashimoto, Keisuke (K); Amano, Taku (T); Sakai, Norio (N); Suzuki, Tsutomu (T); Narita, Minoru (M);
Affiliation: Department of Toxicology, Hoshi University School of Pharmacy and Pharmaceutical Sciences, Tokyo 142-8501, Japan.
Journal and publication information
Publication Type: Journal Article
Journal: Neuroscience letters (Neurosci Lett), published in Ireland. (Language: eng)
Reference: 2009-Feb; vol 451 (issue 3) : pp 270-3
Dates: Created 2009/02/09; Completed 2009/05/20;
PMID: 19159664, status: MEDLINE (last retrieval date: 5/20/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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