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

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  2. Increasing propensity to mind-wander by transcranial direct current stimulation? A registered report

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  3. Comparison of classification methods for tissue outcome after ischaemic stroke

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  4. Blinding is compromised for transcranial direct current stimulation at 1 mA for 20 minutes in young healthy adults

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  5. Individualized quantification of the benefit from reperfusion therapy using stroke predictive models

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  1. Oral D/L-3-Hydroxybutyrate stimulates cholecystokinin and insulin secretion and slows gastric emptying in healthy males

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  2. Bilio-enteric flow and plasma concentrations of bile acids after gastric bypass and sleeve gastrectomy

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  3. Circadian variations in plasma concentrations of cholecystokinin and gastrin in man

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  4. Increased oral sodium chloride intake in humans amplifies selectively postprandial GLP-1 but not GIP, CCK, and gastrin in plasma

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The suprachiasmatic nucleus (SCN) is the principal pacemaker driving circadian rhythms of physiology and behaviour. Neurons within the SCN express both classical and neuropeptide transmitters which regulate clock functions. Cholecyctokinin (CCK) is a potent neurotransmitter expressed in neurons of the mammalian SCN, but its role in circadian timing is not known. In the present study, CCK was demonstrated in a distinct population of neurons located in the shell region of the SCN and in a few cells in the core region. The CCK neurons did not express vasopressin or vasoactive intestinal peptide. However, CCK-containing processes make synaptic contacts with both groups of neurons and some CCK cell bodies were innervated by VIPergic neurons. The CCK neurons received no direct input from the three major pathways to the SCN, and the CCK neurons were not light-responsive as evaluated by induction of cFOS, and did not express the core clock protein PER1. Accordingly, CCK-deficient mice showed normal entrainment and had similar τ, light-induced phase shift and negative masking behaviour as wild-type animals. In conclusion, CCK signalling seems not to be involved directly in light-induced resetting of the clock or in regulating core clock function. The expression of CCK in a subpopulation of neurons, which do not belonging to either the VIP or AVP cells but which have synaptic contacts to both cell types and reverse innervation of CCK neurons from VIP neurons, suggests that the CCK neurons may act in non-photic regulation within the clock and/or, via CCK projections, mediate clock information to hypothalamic nuclei.
Original languageEnglish
JournalEuropean Journal of Neuroscience
Volume32
Issue number6
Pages (from-to)1006-17
Number of pages12
ISSN0953-816X
DOIs
Publication statusPublished - 1 Sep 2010

ID: 31034212