van den Hooff P, Urban I J, de Wied D
Rudolf Magnus Institute for Pharmacology, Medical Faculty, University of Utrecht, The Netherlands.
Brain Res. 1989 Dec 29;505(2):181-6. doi: 10.1016/0006-8993(89)91440-6.
In brain slices of normal Wistar and Long-Evans rats, brief high frequency stimulation of the fimbria fibers induced long-term potentiation (LTP) in excitatory transmission between these fimbria fibers and neurons of the lateral septum (LS). Slices prepared from diabetes insipidus (DI) Brattleboro rats, that contained no vasopressin (VP), consistently failed to maintain LTP in this excitatory transmission. Exogenous VP, administered to slices from DI Brattleboro rats shortly prior to the experiment or released from a subcutaneous depot in DI Brattleboro rats for several days prior to decapitation, corrected this failure. The maintenance of LTP in the LS in slices from Wistar and Long-Evans rats was prevented by D(CH2)5-Tyr(Me)-arginine VP, an antagonist for the V1 type of VP receptors. These results indicate an important role of VP in the maintenance of LTP in excitatory transmission in the LS. It is conjectured that the effects of VP on LS neurons are related to the role of the peptide in the maintenance of LTP and that these processes play a role in memory formation.
在正常Wistar大鼠和Long-Evans大鼠的脑片中，对穹窿纤维进行短暂高频刺激可诱导这些穹窿纤维与外侧隔（LS）神经元之间兴奋性传递的长时程增强（LTP）。由尿崩症（DI）Brattleboro大鼠制备的脑片不含血管加压素（VP），在这种兴奋性传递中始终无法维持LTP。在实验前短时间向DI Brattleboro大鼠脑片施用外源性VP，或在断头前几天从DI Brattleboro大鼠皮下储库释放VP，可纠正这种缺陷。Wistar大鼠和Long-Evans大鼠脑片LS中LTP的维持可被V1型VP受体拮抗剂D(CH2)5-Tyr(Me)-精氨酸VP阻断。这些结果表明VP在LS兴奋性传递中LTP的维持中起重要作用。据推测，VP对LS神经元的作用与该肽在LTP维持中的作用有关，并且这些过程在记忆形成中起作用。
