Cortico-striatal synaptic plasticity in endothelial nitric oxide synthase deficient mice

Nitric oxide (NO) is a retrograde messenger involved in the processes of learning and memory. The role of the endothelial isoform of nitric oxide synthase (eNOS) in striatal synaptic plasticity was investigated in eNOS-deficient (eNOS −/−) and wild type (WT) mice. Tetanic stimulation of cortical aff...

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Published inBrain research Vol. 964; no. 1; pp. 159 - 163
Main Authors Doreulee, Nanuli, Sergeeva, Olga A, Yanovsky, Yevgeni, Chepkova, Aisa N, Selbach, Oliver, Gödecke, Axel, Schrader, Jurgen, Haas, Helmut L
Format Journal Article
LanguageEnglish
Published London Elsevier B.V 21.02.2003
Amsterdam Elsevier
New York, NY
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Summary:Nitric oxide (NO) is a retrograde messenger involved in the processes of learning and memory. The role of the endothelial isoform of nitric oxide synthase (eNOS) in striatal synaptic plasticity was investigated in eNOS-deficient (eNOS −/−) and wild type (WT) mice. Tetanic stimulation of cortical afferents in WT mice evoked either long-term potentiation (LTP), or long-term depression (LTD) of cortico-striatal transmission. Both these plasticity related phenomena were NMDA-receptor-dependent; LTD was blocked by sulpiride, a dopamine D2-receptor antagonist. LTP occurrence in slices from eNOS −/− mice was significantly reduced when compared with WT mice. The NOS inhibitor NL-ARG reduced the occurrence of LTP and increased the occurrence of LTD in WT mice, resembling the balance of LTP/LTD in eNOS −/− mice. Impairment of NO-synthesis thus shifts striatal plasticity towards LTD. This indicates a possible involvement of eNOS from endothelia in neuronal modulation.
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ISSN:0006-8993
1872-6240
DOI:10.1016/S0006-8993(02)04121-5