Signal transmission from the suprachiasmatic nucleus to the pineal gland via the paraventricular nucleus: analysed from arg-vasopressin peptide, rPer2 mRNA and AVP mRNA changes and pineal AA-NAT mRNA after the melatonin injection during light and dark periods

被引:19
作者
Isobe, Y [1 ]
Nishino, H [1 ]
机构
[1] Nagoya City Univ, Grad Sch Med Sci, Dept Neurophysiol & Brain Sci, Nagoya, Aichi 4678601, Japan
关键词
light and dark; clock gene; Bmal1; icer; rat; melatonin;
D O I
10.1016/j.brainres.2004.04.052
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Arg-vasopressin (AVP) containing neurons are one of the output paths from the suprachiasmatic nucleus (SCN), the center of the biological clock. AVP mRNA transcription is controlled by a negative feedback loop of clock genes. Circadian rhythm of melatonin release from the pineal gland is regulated by the SCN via the paraventricular nucleus (PVN). To clarify the transduction system of circadian signals from the SCN to the pineal gland, we determined the effects of melatonin injection (I mg/kg, i.p.) during light and dark periods on Per2 and AVP mRNAs in the SCN and PVN, in addition to arylalkylamine N-acetyltransferase (AA-NAT) and inducible cAMP early repressor (ICER) mRNAs in the pineal gland of rats using RT-PCR. AVP peptide contents were also measured in the SCN and PVN. AVP content in the SCN decreased during the light period, while no changes were observed in the PVN. In the SCN, Per2 mRNA increased during both light and dark periods. In the PVN, Per2 decreased during the light period and increased during the dark period at 180 min after melatonin injection. In the pineal gland, Per2 mRNA increased between 60 and 180 min after the melatonin injection during the light period, while it did not significantly change during the dark period. The AA-NAT mRNA varied similar to the Per2 mRNA changes. These results might suggest that the different responses to melatonin in the pineal gland during the light and dark periods was originated in the changes of Per2 in the PVN via SCN. (C) 2004 Elsevier B.V. All rights reserved.
引用
收藏
页码:204 / 211
页数:8
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