Adenosine A1-receptor agonist attenuates the light-induced phase shifts and fos expression in vivo and optic nerve stimulation-evoked field potentials in the suprachiasmatic nucleus in vitro

Adenosine A1-receptor agonist attenuates the light-induced phase shifts and fos expression in vivo and optic nerve stimulation-evoked field potentials in the suprachiasmatic nucleus in vitro
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腺苷 A1 受体激动剂在体内减弱光诱导的相移和 fos 表达,在体外减弱视神经刺激诱发的视交叉上核场电位

DOI:
10.1016/s0006-8993(96)00881-5
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发表时间:
1996
期刊:
影响因子:
2.9
通讯作者:
Shigenori Watanabe
Shigenori Watanabe
中科院分区:
医学3区
文献类型:
--
作者:
A. Watanabe;T. Moriya;Yukiko Nisikawa;T. Araki;T. Hamada;S. Shibata;Shigenori Watanabe

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腺苷在哺乳动物中枢神经系统中被广泛认为是一种抑制性神经调节剂。在本研究中,我们在体内和体外研究了腺苷受体激动剂是否改变了大鼠视交叉上核的光携带反应。全身给药a1 -腺苷受体激动剂n6 -环己基腺苷(N-CHA)以剂量依赖性方式减弱光(200 lux, 15 min)诱导的仓鼠轮跑节律相移;0.5 mg/kg N-CHA对光致相移的抑制作用为60%。另一方面,a2 -腺苷受体激动剂N6-[2-(3,5-二乙氧基苯基)-2-(2-甲基苯基)-乙基]腺苷(DPMA)未能抑制光诱导的相移。全身给药N-CHA而非DPMA抑制光(300 lux, 1 h)诱导的视交叉上核Fos表达呈剂量依赖性;1 mg/kg N-CHA对光诱导Fos表达的抑制率为73%。N-CHA而非DPMA对大鼠视交叉上核切片视神经刺激诱发场电位有抑制作用。目前的研究结果表明,腺苷a1受体的激活通过抑制视网膜下丘脑通往SCN的通路来减弱光输入。
Adenosine is widely accepted to act as an inhibitory neuromodulator in the mammalian central nervous system. In the present study, we examined whether adenosine receptor agonist modifies the photic entraining responses in the rat suprachiasmatic nucleus both in vivo and in vitro. Light (200 lux, 15 min)-induced phase shifts of hamster wheel-running rhythms was attenuated by a systemic administration of A1-adenosine receptor agonist N6-cyclohexyladenosine (N-CHA) in a dose-dependent manner; 0.5 mg/kg N-CHA caused 60% inhibition of light-induced phase shifts. On the other hand, A2-adenosine receptor agonist N6-[2-(3,5-dirnethoxyphenyl)-2-(2-methyl-phenyl)-ethyl]adenosine (DPMA) failed to inhibit light-induced phase shifts. Systemic administration of N-CHA but not of DPMA inhibited light (300 lux, 1 h)-induced Fos expression in the suprachiasmatic nucleus in a dose-dependent manner; 1 mg/kg N-CHA caused 73% inhibition of light-induced Fos expression. Bath application of N-CHA but not of DPMA inhibited optic nerve stimulation-evoked field potentials in rat suprachiasmatic nucleus slices. The present results suggest that activation of adenosine A1-receptor attenuates the photic input through the inhibition of retinohypotalamic pathway to the SCN.
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