Social deprivation stress is a triggering factor for the emergence of anxiety- and depression-like behaviours and leads to reduced brain BDNF levels in C57BL/6J mice

Berry, Alessandra; Bellisario, Veronica; Capoccia, Sara; Tirassa, Paola; Calza, Arianna; Alleva, Enrico; Cirulli, Francesca

doi:10.1016/j.psyneuen.2011.09.007

Cited by 181 publications

(150 citation statements)

References 65 publications

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“…PD exerts similar effects on hippocampal BDNF levels to maternal deprivation and social isolation [19,20,55,56]. However, BDNF gene expression is increased shortly (on PND 17) after maternal deprivation stress in the hippocampus [20].…”

Section: Discussionmentioning

confidence: 99%

Early Paternal Deprivation Alters Levels of Hippocampal Brain-Derived Neurotrophic Factor and Glucocorticoid Receptor and Serum Corticosterone and Adrenocorticotropin in a Sex-Specific Way in Socially Monogamous Mandarin Voles

Song²,

Wang³

et al. 2014

Neuroendocrinology

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In monogamous mammals, fathers play an important role in the development of the brain and typical behavior in offspring, but the exact nature of this process is not well understood. In particular, little research has addressed whether the presence or absence of paternal care alters levels of hippocampal glucocorticoid receptor (GR) and brain-derived neurotrophic factor (BDNF), and basal levels of serum corticosterone (CORT) and adrenocorticotropin (ACTH). Here, we explored this concept using socially monogamous mandarin voles (Microtus mandarinus), a species in which fathers display high levels of paternal care toward their pups. Our immunohistochemical study shows that paternal deprivation (PD) significantly decreased levels of GR and BDNF protein in the CA1 and CA2/3 of the hippocampus. In the dental gyrus, decreases in GR and BDNF induced by PD were evident in females but not in males. Additionally, enzyme-linked immunosorbent assay results show that PD significantly upregulated levels of serum CORT and ACTH in females, but not males. These findings demonstrate that PD alters HPA axis activity in a sex-specific way. The changes in stress hormones documented here may be associated with alteration in hippocampal BDNF and GR levels.

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Section: Discussionmentioning

confidence: 99%

Early Paternal Deprivation Alters Levels of Hippocampal Brain-Derived Neurotrophic Factor and Glucocorticoid Receptor and Serum Corticosterone and Adrenocorticotropin in a Sex-Specific Way in Socially Monogamous Mandarin Voles

Song²,

Wang³

et al. 2014

Neuroendocrinology

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“…Despite the fact that rodent models are developed for homogeneity across subjects reducing confounding variables, such as genetic modifications and experiential factors (injury variables, individual epigenetic variability, and social housing conditions), that are known to affect depression-like behavior in rodents, there are clear differences in the expression of depression-like behaviors. [78][79][80] The evidence of depression in some subjects, but not others, is intriguing, but is commensurate with the human clinical condition. Indeed, in both human and animal populations, it is clear that not all individuals display all of the symptoms, or even the same constellation of symptoms, of depression.…”

mentioning

confidence: 88%

Assessment of Depression in a Rodent Model of Spinal Cord Injury

Luedtke

Bouchard

Woller

et al. 2014

Journal of Neurotrauma

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Despite an increased incidence of depression in patients after spinal cord injury (SCI), there is no animal model of depression after SCI. To address this, we used a battery of established tests to assess depression after a rodent contusion injury. Subjects were acclimated to the tasks, and baseline scores were collected before SCI. Testing was conducted on days 9-10 (acute) and 19-20 (chronic) postinjury. To categorize depression, subjects' scores on each behavioral measure were averaged across the acute and chronic stages of injury and subjected to a principal component analysis. This analysis revealed a two-component structure, which explained 72.2% of between-subjects variance. The data were then analyzed with a hierarchical cluster analysis, identifying two clusters that differed significantly on the sucrose preference, open field, social exploration, and burrowing tasks. One cluster (9 of 26 subjects) displayed characteristics of depression. Using these data, a discriminant function analysis was conducted to derive an equation that could classify subjects as ''depressed'' on days 9-10. The discriminant function was used in a second experiment examining whether the depression-like symptoms could be reversed with the antidepressant, fluoxetine. Fluoxetine significantly decreased immobility in the forced swim test (FST) in depressed subjects identified with the equation. Subjects that were depressed and treated with saline displayed significantly increased immobility on the FST, relative to not depressed, saline-treated controls. These initial experiments validate our tests of depression, generating a powerful model system for further understanding the relationships between molecular changes induced by SCI and the development of depression.

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“…BDNF plays a major role in the synaptic plasticity associated with learning and memory [11], especially in fear learning and extinction [12]. Anxiety disorders and depression have been associated with decreased levels of BDNF [13,14] or BDNF polymorphisms [15,16]. …”

Section: Anxiety Disorders and Bdnfmentioning

confidence: 99%

Translational Findings on Brain-Derived Neurotrophic Factor and Anxiety: Contributions from Basic Research to Clinical Practice

Luz¹,

Dias²,

Bevilaqua³

et al. 2013

Neuropsychobiology

2,969

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Background/Aims: Anxious responses are evolutionarily adaptive, but excessive fear can become disabling and lead to anxiety disorders. Translational models of anxiety might be useful sources for understanding the neurobiology of fear and anxiety and can contribute to future proposals of therapeutic intervention for the disorders studied. Brain-derived neurotrophic factor (BDNF), which is known for its importance on neuroplasticity and contextual memory, has emerged as a relevant element for emotional memory. Recent studies show that the Val⁶⁶Met BDNF polymorphism correlates with various psychiatric disorders, including anxiety, but there are several differences between experimental and clinical studies. Methods: In this work, we review the literature focused on the BDNF Val⁶⁶Met polymorphism and anxiety, and discuss biological findings from animal models to clinical studies. Results: As occurs with other psychiatric disorders, anxiety correlates with anatomical, behavioral and physiological changes related to the BDNF polymorphism. In animal studies, it has been shown that a significant decrease in regulated secretion from both BDNF_Val/Met and BDNF_Met/Met neurons represented a significant decrease in available BDNF. Conclusion: These studies suggest that developing pharmacological strategies facilitating the release of BDNF from synapses or prolongation of the half-life of secreted BDNF may improve the therapeutic responses of humans expressing the BDNF polymorphism.

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Social deprivation stress is a triggering factor for the emergence of anxiety- and depression-like behaviours and leads to reduced brain BDNF levels in C57BL/6J mice

Cited by 181 publications

References 65 publications

Early Paternal Deprivation Alters Levels of Hippocampal Brain-Derived Neurotrophic Factor and Glucocorticoid Receptor and Serum Corticosterone and Adrenocorticotropin in a Sex-Specific Way in Socially Monogamous Mandarin Voles

Early Paternal Deprivation Alters Levels of Hippocampal Brain-Derived Neurotrophic Factor and Glucocorticoid Receptor and Serum Corticosterone and Adrenocorticotropin in a Sex-Specific Way in Socially Monogamous Mandarin Voles

Assessment of Depression in a Rodent Model of Spinal Cord Injury

Translational Findings on Brain-Derived Neurotrophic Factor and Anxiety: Contributions from Basic Research to Clinical Practice

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