The Journal of Neurophysiology Vol. 82 No. 6 December 1999, pp. 3000-3005
Copyright ©1999 by the American Physiological Society

Selective Modulation of Excitatory Transmission by µ-Opioid Receptor Activation in Rat Supraoptic Neurons

Institute of Neurosciences, The Fourth Military Medical University, Xian 710032, People's Republic of China

Liu, Qing-Song, Sheng Han, You-Sheng Jia, and Gong Ju. Selective Modulation of Excitatory Transmission by µ-Opioid Receptor Activation in Rat Supraoptic Neurons. J. Neurophysiol. 82: 3000-3005, 1999. Opioid peptides have profound inhibitory effects on the production of oxytocin and vasopressin, but their direct effects on magnocellular neuroendocrine neurons appear to be relatively weak. We tested whether a presynaptic mechanism is involved in this inhibition. The effects of µ-opioid receptor agonist D-Ala², N-CH³-Phe⁴, Gly⁵-ol-enkephalin (DAGO) on excitatory and inhibitory transmission were studied in supraoptic nucleus (SON) neurons from rat hypothalamic slices using whole cell recording. DAGO reduced the amplitude of evoked glutamatergic excitatory postsynaptic currents (EPSCs) in a dose-dependent manner. In the presence of tetrodotoxin (TTX) to block spike activity, DAGO also reduced the frequency of spontaneous miniature EPSCs without altering their amplitude distribution, rising time, or decaying time constant. The above effects of DAGO were reversed by wash out, or by addition of opioid receptor antagonist naloxone or selective µ-antagonist Cys²-Tyr³-Orn⁵-Pen⁷-NH₂ (CTOP). In contrast, DAGO had no significant effect on the evoked and spontaneous miniature GABAergic inhibitory postsynaptic currents (IPSCs) in most SON neurons. A direct membrane hyperpolarization of SON neurons was not detected in the presence of DAGO. These results indicate that µ-opioid receptor activation selectively inhibits excitatory activity in SON neurons via a presynaptic mechanism.