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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Behavioral effects of neuropeptide Y in F344 rat substrains with a reduced dipeptidyl-peptidase IV activity.
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Behavioral effects of neuropeptide Y in F344 rat substrains with a reduced dipeptidyl-peptidase IV activity.

机译：二肽基肽酶IV活性降低的F344大鼠亚株中神经肽Y的行为效应。

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摘要

Dipeptidyl-peptidase IV (DPPIV/CD26) is involved in several physiological functions by cleavage of dipeptides with a Xaa-Pro or Xaa-Ala sequence of regulatory peptides such as neuropeptide Y (NPY). Cleavage of NPY by DPPIV results in NPY(3-36), which lacks affinity for the Y(1) but not for other NPY receptor subtypes. Among other effects, the NPY Y(1) receptor mediates anxiolytic-like effects of NPY. In previous studies with F344 rat substrains lacking endogenous DPPIV-like activity we found a reduced behavioral stress response, which might be due to a differential degradation of NPY. Here we tested this hypothesis and administered intracerebroventricularly two different doses of NPY (0.0, 0.2, 1.0 nmol) in mutant and wildtype-like F344 substrains. NPY dose-dependently stimulated food intake and feeding motivation, decreased motor activity in the plus maze and social interaction test, and exerted anxiolytic-like effects. More important for the present hypothesis, NPY administration was found to be morepotent in the DPPIV-negative substrains in exerting anxiolytic-like effects (increased social interaction time in the social interaction test) and sedative-like effects (decreased motor activity in the elevated plus maze). These data demonstrate for the first time a differential potency of NPY in DPPIV-deficient rats and suggest a changed receptor-specificity of NPY, which may result from a differential degradation of NPY in this genetic model of DPPIV deficiency. Overall, these results provide direct evidence that NPY-mediated effects in the central nervous system are modulated by DPPIV-like enzymatic activity.
机译：二肽基肽酶IV（DPPIV / CD26）通过用调节肽如神经肽Y（NPY）的Xaa-Pro或Xaa-Ala序列切割二肽来参与多种生理功能。 DPPIV对NPY的切割会产生NPY（3-36），它对Y（1）缺乏亲和力，但对其他NPY受体亚型没有亲和力。除其他作用外，NPY Y（1）受体介导NPY的抗焦虑样作用。在先前对F344大鼠亚菌株缺乏内源性DPPIV样活性的研究中，我们发现行为应激反应降低，这可能是由于NPY的差异降解所致。在这里，我们测试了这一假设，并在突变型和野生型F344亚菌株中脑室内给予了两种不同剂量的NPY（0.0、0.2、1.0 nmol）。 NPY剂量依赖性地刺激食物的摄取和进食动机，在迷宫和社交互动测试中降低运动活动，并发挥抗焦虑作用。对于当前的假设更重要的是，NPY给药在DPPIV阴性亚株中表现出更强的抗焦虑样作用（在社交互动测试中增加了社交互动时间）和镇静般的效果（在高架运动中运动能力降低）迷宫）。这些数据首次证明了在DPPIV缺乏的大鼠中NPY的差异效力，并暗示了NPY受体特异性的改变，这可能是由于在这种DPPIV缺乏遗传模型中NPY的差异降解所致。总体而言，这些结果提供了直接证据，证明中枢神经系统中NPY介导的作用受DPPIV样酶活性调节。

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