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Previous Article | Next Article
The Journal of Neuroscience, January 1, 1999, 19(1):48-55
Long-Term Potentiation in the Hippocampal CA1 Region of Mice Lacking cGMP-Dependent Kinases Is Normal and Susceptible to Inhibition of Nitric Oxide Synthase
Thomas Kleppisch1, Alexander Pfeifer1, Peter Klatt1, Peter Ruth1, Alexandra Montkowski2, Reinhard Fässler3, and Franz Hofmann1 1 Institut für Pharmakologie und Toxikologie, 80802 München, Germany, 2 Max Planck-Institut für Psychiatrie, 80804 München, Germany, and 3 Department of Experimental Pathology, Lund University Hospital, 22185 Lund, Sweden
Long-term potentiation (LTP) is a potential cellular mechanism for learning and memory. The retrograde messenger nitric oxide (NO) is thought to induce LTP in the CA1 region of the hippocampus via activation of soluble guanylyl cyclase (sGC) and, ultimately, cGMP-dependent protein kinase (cGK). Two genes code for the isozymes cGKI and cGKII in vertebrates. The functional role of cGKs in LTP was analyzed using mice lacking the gene(s) for cGKI, cGKII, or both. LTP was not altered in the mutant mice lineages. However, LTP was reduced by inhibition of NO synthase and NMDA receptor antagonists, respectively. The reduced LTP was not recovered by the cGK-activator 8-(4 chlorophenylthio)-cGMP. Moreover, LTP was not affected by the sGC inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]-quiloxalin-1-one. In contrast, it was effectively suppressed by nicotinamide, a blocker of the ADP-ribosyltransferase. These results show that cGKs are not involved in LTP in mice and that NO induces LTP through an alternative cGMP-independent pathway, possibly ADP-ribosylation.
Key words: synaptic plasticity; hippocampus; nitric oxide; cGMP-dependent kinase; gene targeting; mouse
Copyright © 1999 Society for Neuroscience 0270-6474/99/19148-08$05.00/0
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