Targeted gene deletion of heme oxygenase 2 reveals neural role for carbon monoxide. Academic Article uri icon

Overview

abstract

  • Neuronal nitric oxide synthase (nNOS) generates NO in neurons, and heme-oxygenase-2 (HO-2) synthesizes carbon monoxide (CO). We have evaluated the roles of NO and CO in intestinal neurotransmission using mice with targeted deletions of nNOS or HO-2. Immunohistochemical analysis demonstrated colocalization of nNOS and HO-2 in myenteric ganglia. Nonadrenergic noncholinergic relaxation and cyclic guanosine 3',5' monophosphate elevations evoked by electrical field stimulation were diminished markedly in both nNOSDelta/Delta and HO-2(Delta)/Delta mice. In wild-type mice, NOS inhibitors and HO inhibitors partially inhibited nonadrenergic noncholinergic relaxation. In nNOSDelta/Delta animals, NOS inhibitors selectively lost their efficacy, and HO inhibitors were inactive in HO-2(Delta)/Delta animals.

publication date

  • December 23, 1997

Research

keywords

  • Carbon Monoxide
  • Enteric Nervous System
  • Heme Oxygenase (Decyclizing)
  • Nitric Oxide

Identity

PubMed Central ID

  • PMC25126

Scopus Document Identifier

  • 0031463819

Digital Object Identifier (DOI)

  • 10.1073/pnas.94.26.14848

PubMed ID

  • 9405702

Additional Document Info

volume

  • 94

issue

  • 26