Agonistic encounters in aged male mouse potentiate the expression of endogenous brain NGF and BDNF: possible implication for brain progenitor cells' activation

Fiore, M.; Amendola, Tiziana; Triaca, Viviana; Tirassa, Paola; Alleva, Enrico; Aloe, Luigi

doi:10.1046/j.1460-9568.2003.02573.x

Cited by 49 publications

(22 citation statements)

References 63 publications

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“…Wu et al [128] in social defeat model in mice demonstrated impaired expressions of glucocorticoid receptors mRNA and BDNF mRNA in the hippocampus and increased level of corticotrophin-releasing hormone mRNA in hypothalamus, as well as increased levels of IL-6 and TNF- α in serum. Fiore et al [129] found that dominant animals had higher levels of BDNF mRNA in the subventricular zone and hippocampus than did subordinate animals. Conversely, subordinate animals exhibited higher levels of NGF compared with dominant animals in these neurogenic regions.…”

Section: Stress Exposure During Adulthoodmentioning

confidence: 99%

Rodent Models of Depression: Neurotrophic and Neuroinflammatory Biomarkers

Stepanichev

Дыгало

Grigoryan

et al. 2014

BioMed Research International

144

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Rodent models are an indispensable tool for studying etiology and progress of depression. Since interrelated systems of neurotrophic factors and cytokines comprise major regulatory mechanisms controlling normal brain plasticity, impairments of these systems form the basis for development of cerebral pathologies, including mental diseases. The present review focuses on the numerous experimental rodent models of depression induced by different stress factors (exteroceptive and interoceptive) during early life (including prenatal period) or adulthood, giving emphasis to the data on the changes of neurotrophic factors and neuroinflammatory indices in the brain. These parameters are closely related to behavioral depression-like symptoms and impairments of neuronal plasticity and are both gender- and genotype-dependent. Stress-related changes in expression of neurotrophins and cytokines in rodent brain are region-specific. Some contradictory data reported by different groups may be a consequence of differences of stress paradigms or their realization in different laboratories. Like all experimental models, stress-induced depression-like conditions are experimental simplification of clinical depression states; however, they are suitable for understanding the involvement of neurotrophic factors and cytokines in the pathogenesis of the disease—a goal unachievable in the clinical reality. These major regulatory systems may be important targets for therapeutic measures as well as for development of drugs for treatment of depression states.

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Section: Stress Exposure During Adulthoodmentioning

confidence: 99%

Rodent Models of Depression: Neurotrophic and Neuroinflammatory Biomarkers

Stepanichev

Дыгало

Grigoryan

et al. 2014

BioMed Research International

144

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“…Moreover, aggressive behavior can enhance the number of Ki67-positive cells in the SVZ of aged animals. This suggests that, in the aged mouse, fighting behavior may increase neurogenesis, most probably throughout proliferation and/or differentiation of brain stem cells [86], possibly contributing to reduce the neuronal damage and loss caused by prolonged GC exposure as a consequence of the social stress related to fighting [87, 88]. In addition, within the brain, the major increase in NGF following fighting has been observed in the hypothalamus a brain area involved in the activation of certain behaviors and in physiological modifications inducing changes in bodily homeostasis, suggesting a role for NGF in coping and neuroendocrine mechanisms [31].…”

Section: The Role Of Ngf At the Cnsmentioning

confidence: 99%

NGF, Brain and Behavioral Plasticity

2012

Self Cite

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Nerve Growth Factor (NGF) was initially studied for its role as a key player in the regulation of peripheral innervations. However, the successive finding of its release in the bloodstream of male mice following aggressive encounters and its presence in the central nervous system led to the hypothesis that variations in brain NGF levels, caused by psychosocial stressor, and the related alterations in emotionality, could be functional to the development of proper strategies to cope with the stressor itself and thus to survive. Years later this vision is still relevant, and the body of evidence on the role of NGF has been strengthened and expanded from trophic factor playing a role in brain growth and differentiation to a much more complex messenger, involved in psychoneuroendocrine plasticity.

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“…[3][4][5][6][7][8][9][10][11][12][13][14] In one such in vivo study the growth factor EGF was infused into the lateral ventricle of adult mice; the results demonstrated a dramatic increase in the number of proliferating cells in the subependymal layer of the lateral ventrical. 9 Immunohistochemical analysis revealed that more than 95% of the cells present in the subependymal layer were immunopositive for the EGF receptor and were also nestin positive, a well established marker of proliferating neural progenitor cells.…”

mentioning

confidence: 99%

Neurogenesis in the Diseased Adult Human Brain: New Therapeutic Strategies for Neurodegenerative Diseases

Curtis

Connor²,

Faull³

2003

Cell Cycle

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Worldwide attention is presently focused on the potential use of exogenous progenitor cells as a source of cells for transplantation therapy in neurodegenerative diseases such as Huntington's and Parkinson's disease. Because controversy has surrounded the use of human fetal and embryonic tissue for the purposes of experimentation and transplantation, new sources of cells for transplantation have been sought. Less controversial, and probably more notable, is the recent demonstration of the presence of endogenous progenitor cells in the adult human brain in both the hippocampus and the subependymal layer overlying the caudate nucleus. 1,2 These observations indicate that, contrary to the well rehearsed dogma, the adult human brain contains progenitor cells that are capable of producing new neurons. This raises the possibility that endogenous neural progenitor cells may provide an alternative strategy for cell replacement therapy through the enhancement of endogenous neural replacement mechanisms to produce new neurons that replace the cells that die in neurodegenerative diseases.We have recently demonstrated that in Huntington's disease (a progressive autosomal dominant neurodegenerative disorder that principally affects the striatum) there are significantly more dividing cells in the subependymal layer (the neurogenic layer that overlies the striatum) compared with controls. 2 In this study we have shown that about 5% of the cells that have recently divided become neurons and others become glial cells. In this case, the trigger for the increased cell production in the Huntington's disease brain appears to be the death of neurons in the striatum because as cell death advances in Huntington's disease more dividing cells are present in the subependymal layer of the diseased brain. However, in Huntington's disease it would appear that the increase in cell proliferation and neurogenesis is too little too late. If the proliferation, migration and differentiation of endogenous progenitor cells could be pharmacologically enhanced then progenitor cells may more effectively replace the specific cells that die in neurodegenerative diseases.Neural progenitor cells have been shown to respond to a variety of mitogenic growth/trophic factors and cytokines in vivo such as epidermal growth factor (EGF), fibroblast growth factor (FGF-2), nerve growth factor (NGF), brain derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), erythropoietin (EPO) and others by facilitating the proliferation, migration and differentiation of progenitor cells in the adult central nervous system. [3][4][5][6][7][8][9][10][11][12][13][14] In one such in vivo study the growth factor EGF was infused into the lateral ventricle of adult mice; the results demonstrated a dramatic increase in the number of proliferating cells in the subependymal layer of the lateral ventrical. 9 Immunohistochemical analysis revealed that more than 95% of the cells present in the subependymal layer were immunopositive for the EGF receptor and were also nestin...

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Agonistic encounters in aged male mouse potentiate the expression of endogenous brain NGF and BDNF: possible implication for brain progenitor cells' activation

Cited by 49 publications

References 63 publications

Rodent Models of Depression: Neurotrophic and Neuroinflammatory Biomarkers

Rodent Models of Depression: Neurotrophic and Neuroinflammatory Biomarkers

NGF, Brain and Behavioral Plasticity

Neurogenesis in the Diseased Adult Human Brain: New Therapeutic Strategies for Neurodegenerative Diseases

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