Sosulina Ludmila, Schwesig Gerrit, Seifert Gerald, Pape Hans-Christian
Institut für Physiologie I, Westfälische Wilhelms-Universität Münster, Münster, Germany.
Mol Cell Neurosci. 2008 Nov;39(3):491-8. doi: 10.1016/j.mcn.2008.08.002. Epub 2008 Aug 27.
Neuropeptide Y (NPY) reduces anxiety-related behavior in various animal models. Since activity in the lateral amygdala (LA) seems crucial for fear expression of behavior, we studied the mechanisms of NPY in LA projection neurons using whole-cell patch-clamp recordings in slices of the rat amygdala in vitro. Application of NPY activated a membrane K(+) current with inwardly rectifying properties in 92% of tested neurons. Pharmacological properties were indicative of mediation via Y1 receptors. Nonhydrolyzable analogues of guanine nucleotides and SCH23390 blocked the NPY-activated current. Single-cell RT-PCR demonstrated expression of G-protein-coupled inwardly rectifying K(+) channel (GIRK) subunits GIRK1, GIRK2 and GIRK3, suggesting mediation of the NPY response through GIRK type channels. The NPY-activated current depressed action potential firing in LA projection neurons, through membrane hyperpolarization and decreased input resistance. Functionally, the dampening of excitability in projection neurons of the amygdala may contribute to the decrease in anxiogenic behavior during action of NPY.
神经肽Y（NPY）在多种动物模型中可减少焦虑相关行为。由于外侧杏仁核（LA）的活动对于行为的恐惧表达似乎至关重要，我们利用体外大鼠杏仁核切片的全细胞膜片钳记录技术，研究了NPY在LA投射神经元中的作用机制。在92%的受试神经元中，应用NPY激活了一种具有内向整流特性的膜钾电流。药理学特性表明其通过Y1受体介导。鸟嘌呤核苷酸的不可水解类似物和SCH23390可阻断NPY激活的电流。单细胞逆转录聚合酶链反应（RT-PCR）显示了G蛋白偶联内向整流钾通道（GIRK）亚基GIRK1、GIRK2和GIRK3的表达，提示NPY反应通过GIRK型通道介导。NPY激活的电流通过膜超极化和输入电阻降低抑制了LA投射神经元的动作电位发放。在功能上，杏仁核投射神经元兴奋性的减弱可能有助于NPY作用期间焦虑行为的减少。
