| First Author | Doreulee N | Year | 2003 |
| Journal | Brain Res | Volume | 964 |
| Issue | 1 | Pages | 159-63 |
| PubMed ID | 12573525 | Mgi Jnum | J:81872 |
| Mgi Id | MGI:2450178 | Doi | 10.1016/s0006-8993(02)04121-5 |
| Citation | Doreulee N, et al. (2003) Cortico-striatal synaptic plasticity in endothelial nitric oxide synthase deficient mice. Brain Res 964(1):159-63 |
| abstractText | 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. |
