Affordable Access

Publisher Website

The role of nitric oxide in the proconvulsant effect of δ-opioid agonist SNC80 in mice

Authors
Journal
Neuroscience Letters
0304-3940
Publisher
Elsevier
Publication Date
Volume
329
Issue
2
Identifiers
DOI: 10.1016/s0304-3940(02)00417-2
Keywords
  • Nitric Oxide
  • Nitric Oxide Synthase
  • Delta-Opioid Receptor
  • (+)-4-((Alphar)-Alpha-((2S
  • 5R)-4-Allyl-2
  • 5-Dimethyl-1-Piperazinyl)-3-Methoxybenzyl)-N
  • N-Diethyl-Benzamide
  • Pentylenetetrazole
  • Mice

Abstract

Abstract The involvement of nitric oxide (NO) in modulation of seizure susceptibility by δ-opioid agonist (+)-4-((alpha R)-alpha-((2 S, 5 R)-4-allyl-2, 5-dimethyl-1-piperazinyl)-3-methoxybenzyl)- N, N-diethyl-benzamide (SNC80) was examined in mice. Systemic administration of SNC80 (0.1–5 mg/kg, intraperitoneally (i.p.)) decreased the threshold for clonic seizures induced by pentylenetetrazole. The non-specific NO synthase (NOS) inhibitor, N G-nitro- l-arginine methyl ester (3–20 mg/kg, i.p.), but not the specific inducible NOS inhibitor, aminoguanidine (50 and 100 mg/kg, i.p.) inhibited the proconvulsant effect of SNC80. On the other hand, NO substrate, l-arginine (30 and 60 mg/kg, i.p.) potentiated the proconvulsant effect of a lower dose of SNC80 (0.5 mg/kg). These results support the involvement of NO, produced by constitutive NOS, in the proconvulsant effect of the δ-opioid agonist.

There are no comments yet on this publication. Be the first to share your thoughts.