Very low levels of cholecystokinin octapeptide activate Na-pump in the cerebral cortex of CCK2 receptor-deficient mice

Roots, K., Kairane, C., Salum, T., Kõks, S., Karelson, E., Vasar, E. and Zilmer, M. (2006) Very low levels of cholecystokinin octapeptide activate Na-pump in the cerebral cortex of CCK2 receptor-deficient mice. International Journal of Developmental Neuroscience, 24 (6). pp. 395-400.

Abstract

This study provides the first evidence that CCK-8 (0.01 pM to 0.1 mM) stimulates Na,K-ATPase in the cortical membranes of wild-type and CCK2 receptor-deficient mice. In each genotype, the maximal stimulation was about 40%. Homozygous mice revealed substantially lower EC50 (4 pM) than heterozygous (37 pM) or wild-type animals (682 pM). In homozygous CCK2 receptor-deficient mice, the expression of CCK1 receptor gene was 5-fold higher than in wild-type animals. CCK1 receptor antagonist devazepide counteracted effect of CCK-8 in all three genotypes, whereas CCK2 receptor antagonist L-365, 260 showed significant antagonism in wild-type and heterozygous mice. The cooperativity of Na,K-ATPase for Na+, but not for K+, was lost in homozygous mice. Altogether, very low concentrations of CCK-8 via CCK1 and CCK2 receptors stimulate Na,K-ATPase in the cerebral cortex. CCK2 receptor-deficiency leads to the altered functionality of Na,K-ATPase that might be compensated by CCK1 receptor mediated influence of CCK (and its agonists) on the enzyme.

Item Type:	Journal Article
Publisher:	Elsevier Ltd.
Copyright:	© 2006 ISDN.
URI:	http://researchrepository.murdoch.edu.au/id/eprint/52851

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