Nitric oxide synthase immunoreactivity in the rat hippocampus after status epilepticus induced by perforant pathway stimulation

Brain Res. 2000 Jul 21;871(2):303-10. doi: 10.1016/s0006-8993(00)02487-2.


Nitric oxide has recently been implicated in mediation of neuronal excitotoxicity and damage. This study aimed at elucidating the changes in the expression of neuronal isoform of nitric oxide synthase (nNOS) in the hippocampus after status epilepticus induced by perforant pathway stimulation. nNOS-immunoreactivity (nNOS-ir) and neuronal damage, assessed by silver staining, were evaluated separately in different hippocampal subfields 2 weeks after induction of status epilepticus. Perforant pathway stimulation resulted in an increase in the number of nNOS-immunoreactive neurons in the stratum radiatum of the CA1 and CA3 subfields of the hippocampus proper, and the hilus of the dentate gyrus. The morphology and distribution of the nNOS-ir neurons resembled that of interneurons. No correlation of the number of nNOS-ir neurons to the neuronal damage score was observed. Our results suggest that status epilepticus provokes a de novo expression of nNOS protein, and the nNOS expressing neurons may be selectively resistant to epileptic brain injury.

MeSH terms

  • Animals
  • Cell Count
  • Dentate Gyrus / enzymology
  • Dentate Gyrus / pathology
  • Dentate Gyrus / physiopathology
  • Disease Models, Animal
  • Electric Stimulation
  • Hippocampus / enzymology*
  • Hippocampus / pathology
  • Hippocampus / physiopathology
  • Male
  • Nerve Degeneration / enzymology
  • Nerve Degeneration / pathology
  • Nerve Degeneration / physiopathology
  • Neurons / enzymology
  • Neurons / pathology
  • Nitric Oxide Synthase / metabolism*
  • Perforant Pathway / physiopathology*
  • Rats
  • Rats, Wistar
  • Status Epilepticus / enzymology*
  • Status Epilepticus / pathology
  • Status Epilepticus / physiopathology


  • Nitric Oxide Synthase