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Endocrine, liver-derived IGF-I is of importance for spatial learning and memory in old mice.

Journal article
Authors Johan Svensson
M Diez
Jörgen Engel
Caroline Wass
Åsa Tivesten
John-Olov Jansson
Olle Isaksson
Trevor Archer
Tomas Hökfelt
Claes Ohlsson
Published in The Journal of endocrinology
Volume 189
Issue 3
Pages 617-27
ISSN 0022-0795
Publication year 2006
Published at Institute of Neuroscience and Physiology, Department of Physiology
Department of Psychology
Institute of Neuroscience and Physiology, Department of Pharmacology
Institute of Medicine, Department of Internal Medicine
Pages 617-27
Language en
Links dx.doi.org/10.1677/joe.1.06631
Keywords Aging, physiology, Alzheimer Disease, metabolism, Animals, Female, Immunohistochemistry, methods, In Situ Hybridization, Insulin-Like Growth Factor I, metabolism, Liver, metabolism, Maze Learning, Memory, Mice, Mice, Knockout, Models, Animal, Poly I-C, pharmacology
Subject categories Medical and Health Sciences

Abstract

IGF-I is a neuroprotective hormone, and neurodegenerative disorders, including Alzheimer's disease, have been associated with decreased serum IGF-I concentration. In this study, IGF-I production was inactivated in the liver of adult mice (LI-IGF-I(-/-)), resulting in an approximately 80-85% reduction of circulating IGF-I concentrations. In young (6-month-old) mice there was no difference between the LI-IGF-I(-/-) and the control mice in spatial learning and memory as measured using the Morris water maze test. In old (aged 15 and 18 months) LI-IGF-I(-/-) mice, however, the acquisition of the spatial task was slower than in the controls. Furthermore, impaired spatial working as well as reference memory was observed in the old LI-IGF(-/-) mice. Histochemical analyses revealed an increase in dynorphin and enkephalin immunoreactivities but decreased mRNA levels in the hippocampus of old LI-IGF-I(-/-) mice. These mice also displayed astrocytosis and increased metabotropic glutamate receptor 7a-immunoreactivity. These neurochemical disturbances suggest synaptic dysfunction and early neurodegeneration in old LI-IGF-I(-/-) mice. The decline in serum IGF-I with increasing age may therefore be important for the age-related decline in memory function.

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