Electrophysiological effects of nitric oxide in mouse superior mesenteric ganglion

Bruno Mazet, Steven M. Miller, Joseph H. Szurszewski

Research output: Contribution to journalArticlepeer-review

15 Scopus citations


Effects of nitric oxide (NO) generated from sodium nitroprusside (SNP) on neurons of mouse superior mesenteric ganglion (SMG) were studied in vitro using intracellular recording techniques. SNP solutions caused a membrane hyperpolarization in the majority (64%) of the neurons tested or a hyperpolarization followed by a depolarization in 8% of the neurons tested. The SNP-induced hyperpolarization persisted in a low-Ca2+ high-Mg2+ solution, indicating a direct effect of NO on the postsynaptic membrane. The hyperpolarizing effect of SNP was reduced or abolished by oxyhemoglobin. Electrical stimulation of the colonic nerves evoked a late slow excitatory postsynaptic potential (late sEPSP) in a population of neurons in normal Krebs solution. The amplitude of the late sEPSP was significantly enhanced in the presence of N(G)-nitro-L-arginine, a NO synthase inhibitor. The results, particularly those observed with the NO synthase inhibitor, suggest that endogenous NO was released in the mouse SMG by repetitive nerve stimulation and that it modulated slow synaptic transmission, presumably by a direct action on ganglionic neurons.

Original languageEnglish (US)
Pages (from-to)G324-G331
JournalAmerican Journal of Physiology - Gastrointestinal and Liver Physiology
Issue number2 33-2
StatePublished - 1996


  • electrophysiology
  • slow synaptic transmission
  • sympathetic ganglia

ASJC Scopus subject areas

  • Physiology
  • Hepatology
  • Gastroenterology
  • Physiology (medical)


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