Abstract
Insulin-like growth factor I (IGF-I) is a protein implicated in the regulation of several growth processes. Specifically, IGF-I mediates the action of growth hormone (GH) on its target organs and regulates both the release of somatostatin and GH from the hypothalamus and the release of GH and prolactin from the pituitary gland [1]. Moreover, it exerts a tissue-specific autocrine and paracrine role during the course of normal growth and differentiation [2]. IGF-I also plays a physiological role in the central nervous system (CNS) both during early development and adulthood [3-5]. Alteration in the level of IGF-I during early postnatal life is correlated with several brain dysfunctions [4]. IGF-I appears to participate in normal CNS development by regulating neuronal survival and differentiation and by stimulating glial growth [6]; postnatal synthesis of IGF-I has been detected in brain regions characterised by life-long processes of synapse formation, suggesting an additional role for this peptide in promoting and maintaining neuronal plasticity. Moreover, transgenic mice overexpressing IGF-I have significantly larger brains than controls, likely a result of increased cell size and number [7], while homozygous IGF-I (-/-) mice show reduced brain weights at 2 months of age [8].
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Santucci, D., Luoni, M., Torsello, A., Branchi, I., Mùller, E.E., Alleva, E. (1998). Anti-Insulin-like Growth Factor I Antibodies Affect Locomotion and Passive Avoidance Performances in Sprague-Dawley Rats. In: Müller, E.E. (eds) IGFs in the Nervous System. Springer, Milano. https://doi.org/10.1007/978-88-470-2246-1_12
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DOI: https://doi.org/10.1007/978-88-470-2246-1_12
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