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The Journal of Neuroscience, April 30, 2008, 28(18):4619-4623; doi:10.1523/JNEUROSCI.3410-07.2008

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Brief Communications
Mitogen-Activated Protein Kinase Is a Functional Component of the Autonomous Circadian System in the Suprachiasmatic Nucleus

Makoto Akashi,^1 * Naoto Hayasaka,^3 * Shin Yamazaki,⁴ and Koichi Node²

Departments of ¹Vascular Failure Research and ²Cardiovascular and Renal Medicine, Faculty of Medicine, Saga University, Saga 849-8501, Japan, ³Department of Anatomy and Neurobiology, Kinki University School of Medicine, Osaka-Sayama, Osaka 589-8511, Japan, and ⁴Department of Biological Sciences, Vanderbilt University, Nashville, Tennessee 37235

Correspondence should be addressed to Makoto Akashi, Department of Vascular Failure Research, Saga University Faculty of Medicine, 5-1-1 Nabeshima, Saga 849-8501, Japan. Email: akashima{at}med.saga-u.ac.jp

The suprachiasmatic nucleus (SCN) is the master circadian pacemaker driving behavioral and physiological rhythms in mammals. Circadian activation of mitogen-activated protein kinase [MAPK; also known as ERK (extracellular signal-regulated kinase)] is observed in vivo in the SCN under constant darkness, although the biological significance of this remains unclear. To elucidate this question, we first examined whether MAPK was autonomously activated in ex vivo SCN slices. Moreover, we investigated the effect of MAPK inhibition on circadian clock gene expression and neuronal firing rhythms using SCN-slice culture systems. We show herein that MAPK is autonomously activated in the SCN, and our data demonstrate that inhibition of the MAPK activity results in dampened rhythms and reduced basal levels in circadian clock gene expression at the SCN single-neuron level. Furthermore, MAPK inhibition attenuates autonomous circadian neuronal firing rhythms in the SCN. Thus, our data suggest that light-independent MAPK activity contributes to the robustness of the SCN autonomous circadian system.

Key words: circadian rhythms; ERK; suprachiasmatic nucleus; tissue culture; transcription; transgenic

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Received July 27, 2007; revised Feb. 12, 2008; accepted Feb. 12, 2008.

Correspondence should be addressed to Makoto Akashi, Department of Vascular Failure Research, Saga University Faculty of Medicine, 5-1-1 Nabeshima, Saga 849-8501, Japan. Email: akashima{at}med.saga-u.ac.jp

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