NPY signaling through Y1 receptors modulates thalamic oscillations

NPY signaling through Y1 receptors modulates thalamic oscillations
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DOI:
10.1016/j.peptides.2006.08.043
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发表时间:
2007-02-01
期刊:
影响因子:
3
通讯作者:
Huguenard, John R.
Huguenard, John R.
中科院分区:
医学3区
文献类型:
--
作者:
Brill, Julia;Kwakye, Gunnar;Huguenard, John R.

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神经肽 Y 是 G 蛋白偶联受体家族(Y-1 至 Y-6)的配体。在丘脑中,外源性和内源性释放的 NPY 可以缩短 P13 至 P15 大鼠脑切片中丘脑振荡的持续时间(失神发作的体外模型)。在这里,我们检查哪些 Y 受体参与了这种调节。应用Y-1受体激动剂Leu(31)Pro(34)NPY导致丘脑振荡持续时间可逆性减少(-26.6+/-7.8%),而Y-2受体激动剂肽YY((3-36))和Y-5受体激动剂BWX-46没有发挥显着效果。没有Y受体激动剂影响振荡周期。 Y-1、Y-2和Y-5受体拮抗剂(分别为BIBP3226、BIIE0246和L152,806)的应用产生与从激动剂获得的结果一致的结果。 BIBP3226 引起可逆的去抑制,这种效应会增加振荡持续时间 (18.2 +/- 9.7%),而 BIIE0246 和 L152,806 则没有显着效应。 NPY 的表达仅限于网状丘脑核 (nRt) 中的神经元,但 Y1 受体在 nRt 和相邻丘脑中继核中均表达。因此,nRt内或nRt中继核NPY释放可能导致Y受体介导的丘脑振荡抑制。 (c) 2006 Elsevier Inc. 保留所有权利。
Neuropeptide Y is the ligand of a family of G-protein coupled receptors (Y-1 to Y-6). In the thalamus, exogenous and endogenously released NPY can shorten the duration of thalamic oscillations in brain slices from P13 to P15 rats, an in vitro model of absence seizures. Here, we examine which Y receptors are involved in this modulation. Application of the Y-1 receptor agonist Leu(31)Pro(34)NPY caused a reversible reduction in the duration of thalamic oscillations (-26.6 +/- 7.8%), while the Y-2 receptor agonist peptideYY((3-36)) and the Y-5 receptor agonist BWX-46 did not exert a significant effect. No Y receptor agonist affected oscillation period. Application of antagonists Of Y-1, Y-2 and Y-5, receptors (BIBP3226, BIIE0246 and L152,806, respectively) produced results consistent with those obtained from agonists. BIBP3226 caused a reversible disinhibition, an effect that increases oscillation duration (18.2 +/- 9.7%) while BIIE0246 and L152,806 had no significant effect. Expression of NPY is limited to neurons in the reticular thalamic nucleus (nRt), but Y, receptors are expressed in both nRt and adjacent thalamic relay nuclei. Thus, intra-nRt or nRt to relay nucleus NPY release could cause Y, receptor mediated inhibition of thalamic oscillations. (c) 2006 Elsevier Inc. All rights reserved.