The European journal of neuroscienceAug 25, 2010

Light response and timing control in brain clock neurons that produce cholecystokinin, studied in mice lacking this chemical

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Updated Apr 1, 2026

Abstract

Cholecystokinin (CCK) was identified in a distinct population of neurons in the suprachiasmatic nucleus (SCN) but does not appear to influence light-induced circadian clock resetting.

CCK neurons are located in the shell region of the SCN and a few in the core region.
These CCK neurons do not express vasopressin or vasoactive intestinal peptide.
CCK-containing processes form synaptic connections with both VIP and AVP neurons.
CCK neurons do not receive direct input from the three main pathways leading to the SCN.
These neurons are not responsive to light and do not express the clock protein PER1.
CCK-deficient mice exhibited normal circadian entrainment and similar behavioral responses as wild-type mice.

Simplified

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.

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Light response and timing control in brain clock neurons that produce cholecystokinin, studied in mice lacking this chemical

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