Cholecystokinin (CCK)-expressing neurons in the suprachiasmatic nucleus: innervation, light responsiveness and entrainment in CCK-deficient mice

2010 ◽  
Vol 32 (6) ◽  
pp. 1006-1017 ◽  
Author(s):  
Jens Hannibal ◽  
Christian Hundahl ◽  
Jan Fahrenkrug ◽  
Jens F. Rehfeld ◽  
Lennart Friis-Hansen
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Deficient Mice

scholarly journals Salt-inducible kinase 3 regulates the mammalian circadian clock by destabilizing PER2 protein

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Naoto Hayasaka ◽  
Arisa Hirano ◽  
Yuka Miyoshi ◽  
Isao T Tokuda ◽  
Hikari Yoshitane ◽  
...  
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Cultured Cells ◽  
Ex Vivo ◽  
Phase Variation ◽  
Cycle Phase ◽  
Dark Cycle ◽  
Metabolic Defects ◽  
Locomotor Activities ◽  
Deficient Mice ◽  
Clock Protein

Salt-inducible kinase 3 (SIK3) plays a crucial role in various aspects of metabolism. In the course of investigating metabolic defects in Sik3-deficient mice (Sik3-/-), we observed that circadian rhythmicity of the metabolisms was phase-delayed. Sik3-/- mice also exhibited other circadian abnormalities, including lengthening of the period, impaired entrainment to the light-dark cycle, phase variation in locomotor activities, and aberrant physiological rhythms. Ex vivo suprachiasmatic nucleus slices from Sik3-/- mice exhibited destabilized and desynchronized molecular rhythms among individual neurons. In cultured cells, Sik3-knockdown resulted in abnormal bioluminescence rhythms. Expression levels of PER2, a clock protein, were elevated in Sik3-knockdown cells but down-regulated in Sik3-overexpressing cells, which could be attributed to a phosphorylation-dependent decrease in PER2 protein stability. This was further confirmed by PER2 accumulation in the Sik3-/- fibroblasts and liver. Collectively, SIK3 plays key roles in circadian rhythms by facilitating phosphorylation-dependent PER2 destabilization, either directly or indirectly.

scholarly journals Preservation of light signaling to the suprachiasmatic nucleus in vitamin A-deficient mice

2001 ◽  
Vol 98 (20) ◽  
pp. 11708-11713 ◽  
Author(s):  
C. L. Thompson ◽  
W. S. Blaner ◽  
R. N. Van Gelder ◽  
K. Lai ◽  
L. Quadro ◽  
...  
Keyword(s):  
Vitamin A ◽  
Suprachiasmatic Nucleus ◽  
Light Signaling ◽  
Deficient Mice

Changes in circadian period and morphology of the hypothalamic suprachiasmatic nucleus in fyn kinase-deficient mice

2000 ◽  
Vol 870 (1-2) ◽  
pp. 36-43 ◽  
Author(s):  
Takaki Shima ◽  
Takeshi Yagi ◽  
Yasushi Isojima ◽  
Nobuaki Okumura ◽  
Masato Okada ◽  
...  
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Circadian Period ◽  
Fyn Kinase ◽  
Deficient Mice

scholarly journals Salt-inducible kinase 3 regulates the mammalian circadian clock by destabilizing PER2 protein

2017 ◽  
Author(s):  
Naoto Hayasaka ◽  
Arisa Hirano ◽  
Yuka Miyoshi ◽  
Isao T. Tokuda ◽  
Hikari Yoshitane ◽  
...  
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Cultured Cells ◽  
Ex Vivo ◽  
Phase Variation ◽  
Cycle Phase ◽  
Dark Cycle ◽  
Metabolic Defects ◽  
Locomotor Activities ◽  
Deficient Mice ◽  
Clock Protein

AbstractSalt-inducible kinase 3 (SIK3) plays a crucial role in various aspects of metabolism. In the course of investigating metabolic defects in Sik3-deficient mice (Sik3-/-), we observed that circadian rhythmicity of the metabolisms was phase-delayed. Sik3-/- mice also exhibited other circadian abnormalities, including lengthening of the period, impaired entrainment to the light-dark cycle, phase variation in locomotor activities, and aberrant physiological rhythms. Ex vivo suprachiasmatic nucleus slices from Sik3-/- mice exhibited destabilized and desynchronized molecular rhythms among individual neurons. In cultured cells, Sik3-knockdown resulted in abnormal bioluminescence rhythms. Expression levels of PER2, a clock protein, were elevated in Sik3-knockdown cells but down-regulated in Sik3-overexpressing cells, which could be attributed to a phosphorylation-dependent decrease in PER2 protein stability. This was further confirmed by PER2 accumulation in the Sik3-/- fibroblasts and liver. Collectively, SIK3 plays key roles in circadian rhythms by facilitating phosphorylation-dependent PER2 destabilization, either directly or indirectly.

scholarly journals Circadian Rhythm in Inhibitory Synaptic Transmission in the Mouse Suprachiasmatic Nucleus

2004 ◽  
Vol 92 (1) ◽  
pp. 311-319 ◽  
Author(s):  
Jason Itri ◽  
Stephan Michel ◽  
James A. Waschek ◽  
Christopher S. Colwell
Keyword(s):  
Circadian Rhythm ◽  
Synaptic Transmission ◽  
Suprachiasmatic Nucleus ◽  
Constant Darkness ◽  
Patch Clamp Recording ◽  
Inhibitory Synaptic Transmission ◽  
Whole Cell Patch Clamp ◽  
Light:Dark Cycle ◽  
Brain Slice Preparation ◽  
Deficient Mice

It is widely accepted that most suprachiasmatic nucleus (SCN) neurons express the neurotransmitter GABA and are likely to use this neurotransmitter to regulate excitability within the SCN. To evaluate the possibility that inhibitory synaptic transmission varies with a circadian rhythm within the mouse SCN, we used whole cell patch-clamp recording in an acute brain slice preparation to record GABA-mediated spontaneous inhibitory postsynaptic currents (sIPSCs). We found that the sIPSC frequency in the dorsal SCN (dSCN) exhibited a TTX-sensitive daily rhythm that peaked during the late day and early night in mice held in a light:dark cycle. We next evaluated whether vasoactive intestinal peptide (VIP) was responsible for the observed rhythm in IPSC frequency. Pretreatment of SCN slices with VPAC1/VPAC2- or VPAC2-specific receptor antagonists prevented the increase in sIPSC frequency in the dSCN. The rhythm in sIPSC frequency was absent in VIP/peptide histidine isoleucine (PHI)-deficient mice. Finally, we were able to detect a rhythm in the frequency of inhibitory synaptic transmission in mice held in constant darkness that was also dependent on VIP and the VPAC2 receptor. Overall, these data demonstrate that there is a circadian rhythm in GABAergic transmission in the dorsal region of the mouse SCN and that the VIP is required for expression of this rhythm.

scholarly journals Loss of ZBTB20 impairs circadian output and leads to unimodal behavioral rhythms

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Zhipeng Qu ◽  
Hai Zhang ◽  
Moli Huang ◽  
Guangsen Shi ◽  
Zhiwei Liu ◽  
...  
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Protein Gene ◽  
Zinc Finger Protein ◽  
Adeno Associated Virus ◽  
Behavioral Rhythms ◽  
Zinc Finger Protein Gene ◽  
Finger Protein ◽  
Early Evening ◽  
Nerve System ◽  
Deficient Mice

Many animals display morning and evening bimodal activities in the day/night cycle. However, little is known regarding the potential components involved in the regulation of bimodal behavioral rhythms in mammals. Here, we identified that the zinc finger protein gene Zbtb20 plays a crucial role in the regulation of bimodal activities in mice. Depletion of Zbtb20 in nerve system resulted in the loss of early evening activity, but the increase of morning activity. We found that Zbtb20-deficient mice exhibited a pronounced decrease in the expression of Prokr2 and resembled phenotypes of Prok2 and Prokr2-knockout mice. Injection of adeno-associated virus-double-floxed Prokr2 in suprachiasmatic nucleus could partly restore evening activity in Nestin-Cre; Zbtb20fl/fl (NS-ZB20KO) mice. Furthermore, loss of Zbtb20 in Foxg1 loci, but intact in the suprachiasmatic nucleus, was not responsible for the unimodal activity of NS-ZB20KO mice. Our study provides evidence that ZBTB20-mediated PROKR2 signaling is critical for the evening behavioral rhythms.

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