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* To whom correspondence should be addressed. E-mail: bnsmith{at}tulane.edu.
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 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 pre-labeled with a stomach injection of the transsynaptic retrograde virus expressing EGFP, PRV-152. Solitary tract stimulation resulted in constant latency 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 IPSCs were also reduced in frequency by EM1, but the effect was blocked by tetrodotoxin, 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 DAMGO, and were blocked by naltrexone, CTOP, or 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.
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