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Depression of glutamatergic transmission by nociceptin in the neonatal rat hemisected spinal cord preparation in vitro
Author(s) -
Faber E.S.L.,
Chambers J.P.,
Evans R.H.,
Henderson G.
Publication year - 1996
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1996.tb15969.x
Subject(s) - nociceptin receptor , excitatory postsynaptic potential , population , stimulation , chemistry , glutamatergic , inhibitory postsynaptic potential , spinal cord , neuroscience , (+) naloxone , opioid , opioid receptor , receptor , medicine , endocrinology , pharmacology , biophysics , opioid peptide , biology , glutamate receptor , biochemistry , environmental health
The present study explored the action of nociceptin, the putative endogenous ligand for the orphan opioid receptor (ORL1), on the rat hemisected spinal cord preparation. Electrical stimulation of a dorsal root evokes a glutamatergic population ventral root potential (DR‐VRP) in the corresponding ventral root. Low intensity stimulation evokes two A fibre‐mediated components; a compound action potential of motonuerones superimposed on a population e.p.s.p. (excitatory postsynaptic potential); at higher stimulus intensities sufficient to activate C fibres a more prolonged population e.p.s.p. is evoked. All three components were depressed by nociceptin in a concentration‐dependent manner with IC 50 values (s.e.mean) of 119±2 nM ( n = 4), 241±3 nM ( n = 4) and 32±2 nM ( n = 4), respectively. The depressant actions of nociceptin (30 nM and 300 nM) were not reversed by the opioid antagonist naloxone (1 μ m ). Nociceptin (100 nM and 300 nM) had no effect on the afferent volleys in the dorsal root. Nociceptin therefore appears to be acting as an inhibitory peptide at the spinal level through a naloxone‐insensitive opioid receptor.