title: Agonistic encounters in aged male mouse potentiate the expression of endogenous brain NGF and BDNF: possible implication for brain progenitor cells' activation.
abstract: The condition of dominance or submission following agonistic encounters in the adult male mouse is known to differentially affect brain nerve growth factor, a neurotrophin playing a role in brain remodeling, in the fine tuning of behaviour and in the regulation of the basal forebrain cholinergic neurons. During development and adult life nerve growth factor regulates brain expression of neurotransmitters and the stimulation of progenitor cells (stem cells) which, under different external stimuli, may differentiate into neuronal and/or glial cells promoting the recovery of the injured brain. However, little information is available for the aged brain. Thus in the present study we investigated the effect of the social status ('dominance' vs. 'submission') in the aged mouse on the presence of nerve growth factor, brain-derived neurotrophic factor, choline acetyltransferase, neuropeptide Y and progenitor cells of selected brain regions. We found that aged dominant mice showed increased brain-derived neurotrophic factor in the subventricular zone and hippocampus and increased choline acetyltransferase in the septum and basal nuclei, which were associated with increased presence of progenitor cells in the subventricular zone. Conversely, in aged subordinate mice the data showed a marked brain increase in nerve growth factor in the subventricular zone and hippocampus, choline acetyltransferase in the septum and basal nuclei and neuropeptide Y in the hippocampus and parietal cortex. The possible functional implications of these findings are discussed.
authors.affiliation: Istituto di Neurobiologia e Medicina Molecolare, CNR, viale Marx, 43/15, 00137 Rome, Italy.
authors.forename: Marco
authors.initials: M
authors.lastname: Fiore
authors.forename: Tiziana
authors.initials: T
authors.lastname: Amendola
authors.forename: Viviana
authors.initials: V
authors.lastname: Triaca
authors.forename: Paola
authors.initials: P
authors.lastname: Tirassa
authors.forename: Enrico
authors.initials: E
authors.lastname: Alleva
authors.forename: Luigi
authors.initials: L
authors.lastname: Aloe
mesh_terms: D000375:Aging / Q000502:physiology*; D000378:Agonistic Behavior / Q000502:physiology*; D000818:Animals; D020532:Basal Nucleus of Meynert / Q000378:metabolism; D001522:Behavior, Animal; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics / Q000378:metabolism*; D002552:Cerebral Ventricles / Q000378:metabolism; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D005786:Gene Expression Regulation; D006624:Hippocampus / Q000378:metabolism; D007150:Immunohistochemistry; D007276:Injections, Intraventricular; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D020932:Nerve Growth Factor / Q000235:genetics / Q000378:metabolism*; D009478:Neuropeptide Y / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D012688:Septum Pellucidum / Q000378:metabolism; D013234:Stem Cells / Q000502:physiology*; D013997:Time Factors
chemical_list: D019208:Brain-Derived Neurotrophic Factor; D019394:Ki-67 Antigen; D009478:Neuropeptide Y; D012333:RNA, Messenger; D020932:Nerve Growth Factor; D002795:Choline O-Acetyltransferase