首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Light-induced Fos expression is attenuated in the suprachiasmatic nucleus of serotonin 1B receptor knockout mice.
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Light-induced Fos expression is attenuated in the suprachiasmatic nucleus of serotonin 1B receptor knockout mice.

机译:光诱导的Fos表达在血清素1B受体敲除小鼠的近视眼上核中减弱。

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摘要

The hypothalamic suprachiasmatic nucleus (SCN) is a circadian oscillator that receives a dense serotonergic innervation from the median raphe nucleus. Serotonin (5-HT) modulates the effects of light on circadian behavior by acting on 5-HT1B receptors on retinohypothalamic (RHT) terminals in the SCN. Activation of 5-HT1B presynaptic receptors on RHT terminals inhibits glutamate release. However, 5-HT1B receptor knockout (5-HT1B KO) mice have attenuated behavioral responses to light [P.J. Sollars, M.D. Ogilvie, A.M. Simpson, G.E. Pickard, Photic entrainment is altered in the 5-HT1B receptor knockout mouse, J. Biol. Rhythms 21 (2006) 21-32]. To assess the cellular response of the 5-HT1B KO SCN to light, light-induced Fos expression was analyzed in 5-HT1B KO and wild-type (WT) mice. In addition, the distribution of melanopsin containing retinal ganglion cells that contribute the majority of axons to the RHT was examined in 5-HT1B KO mice and compared to that of WT mice. Light-induced Fos expression in the SCN was reduced in 5-HT1B KO mice compared to WT mice at circadian time (CT) 16 and CT 23 in a manner similar to the reduction previously described in light-induced behavioral phase shifts. The number of melanopsin retinal ganglion cells was similar in WT and 5-HT1B KO mice. These data taken together with previous data suggest that functional removal of the 5-HT1B receptor results in reduced functional light input to the SCN.
机译:下丘脑上交叉晶状体核(SCN)是一种昼夜节律振荡器,可从正中睑裂核接受密集的血清素能神经支配。 5-羟色胺(5-HT)通过作用于SCN视网膜下丘脑(RHT)末端上的5-HT1B受体来调节光对生物钟行为的影响。 RHT末端上的5-HT1B突触前受体的激活抑制了谷氨酸的释放。然而,5-HT1B受体敲除(5-HT1B KO)小鼠对光的行为反应减弱。 Sollars,M.D. Ogilvie,A.M.辛普森(GE) Pickard,5-HT1B受体基因敲除小鼠,J.Biol.Chem.Sci。,1994,5,4,3,4,4,4,4,4,4,4,4,4,5,4,4,4,4,4,4,4,4,4,4,4,4,3,4,4,6,3,4,3,3,4,4,6,3,4,3,4,6,6,8,9,8,9,8,9,8,9,8,9,8,9,9。 Rhythms 21(2006)21-32]。为了评估5-HT1B KO SCN对光的细胞反应,在5-HT1B KO和野生型(WT)小鼠中分析了光诱导的Fos表达。另外,在5-HT1B KO小鼠中检查了包含大多数轴突对RHT的含黑色素的视网膜神经节细胞的分布,并与WT小鼠进行了比较。在昼夜时间(CT)16和CT 2​​3,与WT小鼠相比,5-HT1B KO小鼠中SCN中光诱导的Fos表达降低,其方式类似于先前在光诱导行为相移中描述的降低方式。在WT和5-HT1B KO小鼠中,黑视蛋白视网膜神经节细胞的数量相似。这些数据与以前的数据一起表明5-HT1B受体的功能性去除导致输入SCN的功能光减少。

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