Kask A, Rägo L, Harro J
Department of Pharmacology, University of Tartu, Estonia.
Neuroreport. 1997 Nov 10;8(16):3645-7. doi: 10.1097/00001756-199711100-00044.
We reported previously that the neuropeptide Y (NPY) Y1 receptor antagonist, N2-(diphenylacetyl)-N-[(4-hydroxy-phenyl)methyl]-D-arginine amide (BIBP3226) has an anxiogenic-like effect in the elevated plus maze test in rats. In this study we investigated the effect of the corticotropin-releasing factor (CRF) receptor antagonist, alpha-helical-CRF(9-41) (alpha-h-CRF) on this response. BIBP3226 (5 microg, i.c.v.) induced an anxiogenic-like effect, which was blocked by pretreatment with alpha-h-CRF at a concentration (1 microg, i.c.v.) which alone failed to affect the elevated plus maze performance. Thus, the anxiogenic effect of a selective Y1 receptor blocker was prevented by the blockade of CRF receptors, suggesting antagonistic effects of endogenous NPY and CRF in shaping the response to novelty.
我们之前报道过，神经肽Y（NPY）Y1受体拮抗剂N2-（二苯乙酰基）-N-[(4-羟基苯基)甲基]-D-精氨酸酰胺（BIBP3226）在大鼠高架十字迷宫试验中具有类焦虑样效应。在本研究中，我们调查了促肾上腺皮质激素释放因子（CRF）受体拮抗剂α-螺旋-CRF(9-41)（α-h-CRF）对该反应的影响。BIBP3226（5微克，脑室内注射）诱导出类焦虑样效应，而在单独使用时未能影响高架十字迷宫行为表现的浓度（1微克，脑室内注射）下预先给予α-h-CRF可阻断该效应。因此，通过阻断CRF受体可防止选择性Y1受体阻断剂的致焦虑效应，这表明内源性NPY和CRF在塑造对新事物的反应中具有拮抗作用。
