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  • Title: Nociceptin-induced outward current in substantia gelatinosa neurones of the adult rat spinal cord.
    Author: Luo C, Kumamoto E, Furue H, Yoshimura M.
    Journal: Neuroscience; 2001; 108(2):323-30. PubMed ID: 11734364.
    Abstract:
    Nociceptin (NOC), also known as orphanin FQ, is a newly discovered endogenous ligand for the opioid receptor-like1 (ORL1) receptor. Although NOC has been shown to modulate nociceptive transmission, mechanisms for this action are still unknown. In the present study, actions of NOC on substantia gelatinosa (SG) neurones were examined in adult rat spinal cord slice preparations by using the whole-cell patch-clamp technique. NOC at a concentration of 1 microM induced an outward current having an amplitude of 26+/-5 pA (n=68) at a holding potential of -70 mV; this action was dose-dependent with an EC(50) value of 0.23 microM (Hill coefficient: 1.5). The NOC current reversed its polarity at a potential which was close to the equilibrium potential for K(+), as calculated by the Nernst equation (n=4). The NOC current had slope conductances of 0.80+/-0.15 nS and 0.50+/-0.13 nS (n=4) in voltage ranges of -120 to -140 mV and of -60 to -90 mV, respectively. The NOC current was inhibited by Ba(2+) (100 microM; by 56+/-8%, n=4) but not by 4-aminopyridine (4-AP; 1 mM; n=4) and tetraethylammonium (TEA; 5 mM; n=4). The NOC current was not affected by tetrodotoxin (TTX; 1 microM; n=4) and also by a non-specific opioid receptor antagonist, naloxone (1 microM; n=4). When examined using some inhibitors with respect to the ORL1 receptor, the NOC (1 microM) current was depressed in amplitude by a putative NOC precursor product, nocistatin (1 microM; by 18+/-4%, n=6) and also by a non-peptidyl ORL1 receptor antagonist, CompB (1 microM; by 64+/-10%, n=7) without a change in holding currents. On the other hand, a putative ORL1 receptor antagonist, [Phe(1)psi(CH(2)-NH)Gly(2)]nociceptin-(1-13)-NH(2) (1 microM; which is a derivative of NOC), by itself induced an outward current (7+/-3 pA, n=8), during which the NOC current was suppressed in amplitude by 56+/-8% (n=8). We conclude that NOC activates in SG neurones a K(+) channel exhibiting a mild inwardly rectification through the activation of ORL1 receptor; this hyperpolarising action of NOC might contribute to at least a part of its antinociceptive effect.
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