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Release of Neuropeptide FF, an Anti‐Opioid Peptide, in Rat Spinal Cord Slices Is Voltage‐ and Ca 2+ ‐Sensitive: Possible Involvement of P‐Type Ca 2+ Channels
Author(s) -
Devillers J.P.,
Labrouche S. A.,
Castes E.,
Simonnet G.
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.64041567.x
Subject(s) - chemistry , veratridine , voltage dependent calcium channel , biophysics , calcium channel , diltiazem , depolarization , nimodipine , neuropeptide , spinal cord , nifedipine , calcium , endocrinology , medicine , receptor , sodium channel , neuroscience , biochemistry , sodium , biology , organic chemistry
Neuropeptide FF (NPFF), an FMRFamide‐like peptide with antiopioid properties, inhibits morphine‐induced analgesia but also produces hyperalgesia. In the present study, the mechanisms of NPFF release were investigated in an in vitro superfusion system with rat spinal cord slices. The opening of voltage‐sensitive Na + channels with veratridine (20 µ M ) induced calcium‐dependent NPFF release, which was abolished by tetrodotoxin (1 µ M ), suggesting that NPFF release depends on nerve impulse activity. We also showed that NPFF release was a function of the extent of depolarization and was calcium dependent. The 30 m M K + ‐induced release was blocked by Co 2+ or Ni 2+ (2.5 m M ) but was unaffected by Ca 2+ channel blockers of the L type—Cd 2+ (100 µ M ), nifedipine or nimodipine (10 µ M ), diltiazem (20 µ M ), or verapamil (50 µ M )—or the N type—ω‐conotoxin GVIA (1 µ M ). In contrast, ω‐agatoxin IVA (1 µ M ) led to a 65% reduction in NPFF release, suggesting that P‐type Ca 2+ channels play a prominent role. The 35% remaining release resulted from activation of an unknown subtype. The NPFF‐like material in superfusates recognized spinal NPFF receptors, suggesting that NPFF release in the spinal cord has a physiological role.