title: Modulation of fibroblast growth factor-2 by stress and corticosteroids: from developmental events to adult brain plasticity.
abstract: Neurotrophic factors are a heterogeneous group of peptides that play important roles on brain function at different development stages. Basic fibroblast growth factor (FGF-2), one of these molecules, is highly expressed in developing and adult brain. Its expression can be regulated under different experimental situations and this may be relevant for cellular vulnerability and brain plasticity. Stress and glucocorticoid hormones produce short- and long-term effects on brain function, which can involve the regulation of specific neurotrophic factors within selected brain structures. Treatments with corticosterone or dexamethasone up-regulate FGF-2 expression in different rat brain regions as well as in cultured astroglial cells. A similar elevation of FGF-2 biosynthesis is also observed in several brain regions following an acute restraint stress. This response is rapid and transient and, as FGF-2 is neuroprotective, may represent a defense mechanism through which the brain may limit the deleterious effect of stress over time. Moreover exposure to corticosterone during late stage of embryonic life (E18-E20) produces a significant reduction of FGF-2 mRNA levels in the adult hippocampus of male rats as well as changes in its acute modulation in response to stress or corticosterone. These data suggest that stress-related events taking place during brain maturation can modulate the expression of FGF-2 within selected brain regions thus contributing to permanent structural and functional alterations leading to an increased vulnerability to challenging life events.
authors.affiliation: Center of Excellence for Neurodegenerative Disorders, University of Milan, Via Balzaretti 9, 20133, Milan, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Molteni
authors.forename: F
authors.initials: F
authors.lastname: Fumagalli
authors.forename: V
authors.initials: V
authors.lastname: Magnaghi
authors.forename: M
authors.initials: M
authors.lastname: Roceri
authors.forename: M
authors.initials: M
authors.lastname: Gennarelli
authors.forename: G
authors.initials: G
authors.lastname: Racagni
authors.forename: R C
authors.initials: RC
authors.lastname: Melcangi
authors.forename: M A
authors.initials: MA
authors.lastname: Riva
mesh_terms: D000305:Adrenal Cortex Hormones / Q000378:metabolism* / Q000494:pharmacology; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000196:embryology / Q000254:growth & development / Q000378:metabolism*; D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000235:genetics / Q000378:metabolism*; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism; D008297:Male; D051379:Mice; D009414:Nerve Growth Factors / Q000378:metabolism; D009473:Neuronal Plasticity / Q000502:physiology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D013312:Stress, Physiological / Q000378:metabolism*
chemical_list: D000305:Adrenal Cortex Hormones; D009414:Nerve Growth Factors; D012333:RNA, Messenger; D016222:Fibroblast Growth Factor 2