title: Cortico-striatal synaptic plasticity in endothelial nitric oxide synthase deficient mice.
abstract: 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.
authors.affiliation: Department of Physiology II, Heinrich-Heine-Universität, POB 101007, D-40001 Düsseldorf, Germany.
authors.forename: Nanuli
authors.initials: N
authors.lastname: Doreulee
authors.forename: Olga A
authors.initials: OA
authors.lastname: Sergeeva
authors.forename: Yevgeni
authors.initials: Y
authors.lastname: Yanovsky
authors.forename: Aisa N
authors.initials: AN
authors.lastname: Chepkova
authors.forename: Oliver
authors.initials: O
authors.lastname: Selbach
authors.forename: Axel
authors.initials: A
authors.lastname: Gödecke
authors.forename: Jurgen
authors.initials: J
authors.lastname: Schrader
authors.forename: Helmut L
authors.initials: HL
authors.lastname: Haas
mesh_terms: D000818:Animals; D002540:Cerebral Cortex / Q000166:cytology / Q000201:enzymology* / Q000254:growth & development; D018492:Dopamine Antagonists / Q000494:pharmacology; D065127:Dopamine D2 Receptor Antagonists; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005260:Female; D007858:Learning / Q000502:physiology; D017774:Long-Term Potentiation / Q000187:drug effects / Q000502:physiology; D036881:Long-Term Synaptic Depression / Q000187:drug effects / Q000502:physiology; D008297:Male; D008568:Memory / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D017072:Neostriatum / Q000166:cytology / Q000201:enzymology* / Q000254:growth & development; D009473:Neuronal Plasticity / Q000502:physiology*; D009569:Nitric Oxide / Q000096:biosynthesis*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000172:deficiency* / Q000235:genetics; D017448:Receptors, Dopamine D2 / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects / Q000378:metabolism; D013569:Synapses / Q000201:enzymology*
chemical_list: D018492:Dopamine Antagonists; D065127:Dopamine D2 Receptor Antagonists; D004791:Enzyme Inhibitors; D018691:Excitatory Amino Acid Antagonists; D017448:Receptors, Dopamine D2; D016194:Receptors, N-Methyl-D-Aspartate; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase