Effects of endomorphin on substantia gelatinosa neurons in rat spinal cord slices

Su-Ying Wu, Yoshitaka Ohtubo, G Cristina Brailoiu, Nae J Dun
British Journal of Pharmacology 2003, 140 (6): 1088-96
1. Whole-cell patch recordings were made from substantia gelatinosa (SG) neurons in transverse lumbar spinal cord slices of 15- to 30-day-old rats. 2. Endomorphin 1 (EM-1) or EM-2 (<or=10 microM) hyperpolarized or induced an outward current in 26 of the 66 SG neurons. The I-V relationship showed that the peptide activates an inwardly rectifying K+ current. 3. EM-1 or EM-2 (0.3-10 microM) suppressed short-latency excitatory postsynaptic currents (EPSCs) and long-latency inhibitory postsynaptic currents (IPSCs) in nearly all SG neurons tested or short-latency IPSCs in six of the 10 SG neurons. [Met5] enkephalin or [d-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin (DAMGO) (1-10 microM) depressed EPSCs and IPSCs. EM-1 or EM-2 depressed synaptic responses without causing a significant change in holding currents or inward currents induced by glutamate. 4. Glutamate also evoked a short-latency outward current in five SG neurons or a biphasic current in two neurons; the outward current was blocked by tetrodotoxin (TTX, 0.3 microM) or bicuculline (10 microM). 5. EM-1 or DAMGO (1 or 5 microM) attenuated the glutamate-evoked outward or biphasic currents in four of the seven SG neurons. EM-1 (1 microm) reduced the frequency, but not the amplitude of miniature EPSCs or miniature IPSCs. 6.. Naloxone (1 microM) or the selective micro-opioid receptor antagonist beta-funaltrexamine (beta-FNA, 25 microM) antagonized the action of EM; EM-induced hyperpolarizations persisted in the presence of the kappa-opioid receptor antagonist (nor-binaltorphimine dihydrochloride, 1 microM) and/or sigma-opioid receptor antagonist (naltrindole hydrochloride, 1 microM). 7. It may be concluded that EM acting on micro-opioid receptors hyperpolarizes a population of SG neurons by activating an inwardly rectifying K+ current, and attenuates excitatory and inhibitory synaptic currents evoked in a population of SG neurons, probably by a presynaptic site of action.

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