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This Article Full Text Full Text (PDF) All Versions of this Article: 93/5/2530    most recent 00429.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science 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 ISI Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Glatzer, N. R. Articles by Smith, B. N. Search for Related Content PubMed PubMed Citation Articles by Glatzer, N. R. Articles by Smith, B. N.

Modulation of Synaptic Transmission in the Rat Nucleus of the Solitary Tract by Endomorphin-1

Department of Cell and Molecular Biology, Division of Neurobiology, Tulane University, New Orleans, Louisiana

Submitted 27 April 2004; accepted in final form 15 December 2004

Activation of opioid receptors in the periphery and centrally in the brain results in inhibition of gastric and other vagally mediated functions. The aim of this study was to examine the role of the endogenous opioid agonist endomorphin 1 (EM-1) in regulating synaptic transmission within the nucleus tractus solitarius (NTS), an integration site for autonomic functions. We performed whole cell patch-clamp recordings from coronal brain slices of the rat medulla. A subset of the neurons studied was prelabeled with a stomach injection of the transsynaptic retrograde virus expressing EGFP, PRV-152. Solitary tract stimulation resulted in constant latency excitatory postsynaptic currents (EPSCs) that were decreased in amplitude by EM-1 (0.01–10 µM). The paired-pulse ratio was increased with little change in input resistance, suggesting a presynaptic mechanism. Spontaneous EPSCs were decreased in both frequency and amplitude by EM-1, and miniature EPSCs were reduced in frequency but not amplitude, suggesting a presynaptic mechanism for the effect. Spontaneous inhibitory postsynaptic currents (IPSCs) were also reduced in frequency by EM-1, but the effect was blocked by TTX, suggesting activity at receptors on the somata of local inhibitory neurons. Synaptic input arising from local NTS neurons, which were activated by focal photolysis of caged glutamate, was inhibited by EM-1. The actions of EM-1 were similar to those of D-Ala², N-Me-Phe⁴, Gly⁵-ol]-enkephalin (DAMGO) and were blocked by naltrexone, D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH₂ (CTOP), or D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH₂ (CTAP). These results suggest that EM-1 acts at µ-opioid receptors to modulate viscerosensory input and specific components of local synaptic circuitry in the NTS.

This article has been cited by other articles:

				N. R. Glatzer, A. V. Derbenev, B. W. Banfield, and B. N. Smith Endomorphin-1 Modulates Intrinsic Inhibition in the Dorsal Vagal Complex J Neurophysiol, September 1, 2007; 98(3): 1591 - 1599. [Abstract] [Full Text] [PDF]

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