Molsidomine modulates the cNOS activity in an experimental model of cholinergic damage induced by 192-IgG saporin

Neurosci Lett. 2011 Mar 17;491(2):133-7. doi: 10.1016/j.neulet.2011.01.023. Epub 2011 Jan 13.

Abstract

The aim of this work was to study the effect of molsidomine (MOLS), a nitric oxide (NO) donor, on the nitrergic system changes in an experimental model of cholinergic damage induced by 192 IgG saporin (SAP). Male rats were injured by intraseptal administration of SAP (0.22 μg), after seven days, rats were administered with MOLS (4 mg/kg, i.p.) 60 min before sacrifice. Prefrontal cortex (PC), striatum (S) and hippocampus (HC) were dissected out. Results showed significant recovery of the constitutive NOS activity (cNOS) in PC and S regions by MOLS but not in HC compared against controls. SAP reduced the cellular population in the lesion site and MOLS was able to avoid the progression of damage in this area. NO donor is able to modulate the nitrergic status in an experimental model induced by SAP.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / toxicity
  • Brain / drug effects*
  • Brain / metabolism*
  • Cholinergic Agents / toxicity
  • Male
  • Molsidomine / pharmacology*
  • Nitric Oxide Donors / pharmacology*
  • Nitric Oxide Synthase / metabolism*
  • Rats
  • Rats, Wistar
  • Ribosome Inactivating Proteins, Type 1 / toxicity
  • Saporins

Substances

  • 192 IgG-saporin
  • Antibodies, Monoclonal
  • Cholinergic Agents
  • Nitric Oxide Donors
  • Ribosome Inactivating Proteins, Type 1
  • Molsidomine
  • Nitric Oxide Synthase
  • Saporins