title: Effects of endomorphin on substantia gelatinosa neurons in rat spinal cord slices.
abstract: 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.
authors.affiliation: Department of Pharmacology, James H Quillen College of Medicine, East Tennessee State University, PO Box 70577, Johnson City, TN 37614, USA.
authors.forename: Su-Ying
authors.initials: SY
authors.lastname: Wu
authors.forename: Yoshitaka
authors.initials: Y
authors.lastname: Ohtubo
authors.forename: G Cristina
authors.initials: GC
authors.lastname: Brailoiu
authors.forename: Nae J
authors.initials: NJ
authors.lastname: Dun
mesh_terms: D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)- / Q000494:pharmacology; D004745:Enkephalins / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects; D005260:Female; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009270:Naloxone / Q000494:pharmacology; D009271:Naltrexone / Q000031:analogs & derivatives* / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D009842:Oligopeptides / Q000494:pharmacology*; D018408:Patch-Clamp Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D017450:Receptors, Opioid, mu / Q000819:agonists / Q000037:antagonists & inhibitors / Q000502:physiology*; D013116:Spinal Cord / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D013376:Substantia Gelatinosa / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology; D013997:Time Factors
chemical_list: D004745:Enkephalins; D009292:Narcotic Antagonists; D009842:Oligopeptides; D017450:Receptors, Opioid, mu; C105293:endomorphin 1; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; D009270:Naloxone; C105294:endomorphin 2; D013779:Tetrodotoxin; D009271:Naltrexone; C024524:beta-funaltrexamine; D001640:Bicuculline