Hippocampal long-term potentiation is normal in heme oxygenase-2 mutant mice.

Published

Journal Article

We have generated mice deficient in HO-2, the major cerebral isoform of heme oxygenase, in order to assess the potential role of carbon monoxide as a retrograde messenger in hippocampal LTP. Cerebral HO catalytic activity was markedly reduced in the HO-2 mutant mice, yet no differences were found between wild types and mutants in gross neuroanatomical structure, in basal hippocampal synaptic transmission, or in the amount of potentiation produced by various LTP induction protocols. Furthermore, zinc protoporphyrin IX, an inhibitor of HO, had nearly identical inhibitory effects on LTP in wild-type and HO-2 mutant hippocampal slices. Our data indicate that carbon monoxide produced endogenously by HO is unlikely to be a neuromodulator required for LTP in the hippocampus.

Full Text

Duke Authors

Cited Authors

  • Poss, KD; Thomas, MJ; Ebralidze, AK; O'Dell, TJ; Tonegawa, S

Published Date

  • October 1995

Published In

Volume / Issue

  • 15 / 4

Start / End Page

  • 867 - 873

PubMed ID

  • 7576635

Pubmed Central ID

  • 7576635

International Standard Serial Number (ISSN)

  • 0896-6273

Language

  • eng

Conference Location

  • United States