Fluoxetine-induced change in rat brain expression of brain-derived neurotrophic factor varies depending on length of treatment

Foubert, G. de; Carney, Stephen; Robinson, Christine S.; Destexhe, Éric; Tomlinson, Rosemarie; Hicks, Caroline; Murray, Tracey K.; Gaillard, J; Deville, Claude; Xhenseval, Valérie; Thomas, Craig E.; O’Neill, Michael; Zetterström, T.

doi:10.1016/j.neuroscience.2004.06.054

Cited by 227 publications

(150 citation statements)

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“…Reasons for this may in some way be due to the fact that whole tissue homogenate may dilute potential effects at the mRNA levels that occur only in specific subregions of the hippocampus, however this reasoning is unsatisfactory as it should also apply to regulation at the protein level. Moreover, in agreement with our findings, recent studies have also shown very disparate results between BDNF mRNA and protein levels in the same tissue following various antidepressant manipulations mGluR7 modulates HPA axis K Mitsukawa et al (De Foubert et al, 2004;Jacobsen and Mork, 2004). The reasons for such differential responses at mRNA and protein level are currently unclear and warrant further investigation and possibly reflect regulation of BDNF at the translational level.…”

Section: Discussionsupporting

confidence: 91%

“…Intracerebral ventricular or intrahippocampal administration of BDNF has been shown to have an antidepressant-like effect in various animal tests of antidepressant activity (Siuciak et al, 1997;Shirayama et al, 2002;Hoshaw et al, 2005). Furthermore, antidepressant medications have been shown to increase BDNF levels in the hippocampus (Nibuya et al, 1995;De Foubert et al, 2004;Russo-Neustadt et al, 2004; but see Altar et al, 2003;Coppell et al, 2003;Jacobsen and Mork, 2004). Further evidence for a role of BDNF in antidepressant action comes from studies using genetically modified mice with impaired levels of BDNF or its receptor TRK-B, which are resistant to the behavioral effects of antidepressants (Saarelainen et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

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Metabotropic Glutamate Receptor Subtype 7 Ablation Causes Dysregulation of the HPA Axis and Increases Hippocampal BDNF Protein Levels: Implications for Stress-Related Psychiatric Disorders

Mitsukawa

Mombereau

Lötscher

et al. 2005

Neuropsychopharmacol

125

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Regulation of neurotransmission via group-III metabotropic glutamate receptors (mGluR4, -6, -7, and -8) has recently been implicated in the pathophysiology of affective disorders, such as major depression and anxiety. For instance, mice with a targeted deletion of the gene for mGluR7 (mGluR7 À/À ) showed antidepressant and anxiolytic-like effects in a variety of stress-related paradigms, including the forced swim stress and the stress-induced hyperthermia tests. Deletion of mGluR7 reduces also amygdala-and hippocampus-dependent conditioned fear and aversion responses. Since the hypothalamic-pituitary-adrenal (HPA) axis regulates the stress response we investigate whether parameters of the HPA axis at the levels of selected mRNA transcripts and endocrine hormones are altered in mGluR7-deficient mice. Over all, mGluR7 À/À mice showed only moderately lower serum levels of corticosterone and ACTH compared with mGluR7 + / + mice. More strikingly however, we found strong evidence for upregulated glucocorticoid receptor (GR)-dependent feedback suppression of the HPA axis in mice with mGluR7 deficiency: (i) mRNA transcripts of GR were significantly upregulated in the hippocampus of mGluR7 À/À animals, (ii) similar increases were seen with 5-HT 1A receptor transcripts, which are thought to be directly controlled by the transcription factor GR and finally (iii) mGluR7 À/À mice showed elevated sensitivity to dexamethasone-induced suppression of serum corticosterone when compared with mGluR7 + / + animals. These results indicate that mGluR7 deficiency causes dysregulation of HPA axis parameters, which may account, at least in part, for the phenotype of mGluR7 À/À mice in animal models for anxiety and depression. In addition, we present evidence that protein levels of brain-derived neurotrophic factor are also elevated in the hippocampus of mGluR7 À/À mice, which we discuss in the context of the antidepressant-like phenotype found in those animals. We conclude that genetic ablation of mGluR7 in mice interferes at multiple sites in the neuronal circuitry and molecular pathways implicated in affective disorders.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Metabotropic Glutamate Receptor Subtype 7 Ablation Causes Dysregulation of the HPA Axis and Increases Hippocampal BDNF Protein Levels: Implications for Stress-Related Psychiatric Disorders

Mitsukawa

Mombereau

Lötscher

et al. 2005

Neuropsychopharmacol

125

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“…Thus, the possible slower production of BDNF protein in RLA versus RHA rats, as also suggested by the lower density of BDNF‐LI in the dentate gyrus of the ventral hippocampus, may in turn lead to a reduced target‐derived support to promote the synaptic contacts with the mossy fibers. Interestingly, a selective increase in both BDNF mRNA and protein in the CA3 and CA2 sectors has been reported upon repeated antidepressant treatment (De Foubert et al., 2004). The significantly lower density of trkB immunoreactivity observed in the dentate gyrus of the dorsal hippocampus of RLA versus RHA rats further suggests that the functional tone of BDNF‐trkB signaling in the dentate gyrus may be less intense in RLA rats as compared to their RHA counterparts.…”

Section: Discussionmentioning

confidence: 99%

Expression of BDNF and trkB in the hippocampus of a rat genetic model of vulnerability (Roman low‐avoidance) and resistance (Roman high‐avoidance) to stress‐induced depression

et al. 2017

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IntroductionThe selective breeding of Roman High‐ (RHA) and Low‐Avoidance (RLA) rats for, respectively, rapid versus poor acquisition of the active avoidance response has generated two distinct phenotypes differing in many behavioral traits, including coping strategies to aversive conditions. Thus, RLA rats are considered as a genetic model of vulnerability to stress‐induced depression whereas RHA rats are a model of resilience to that trait. Besides the monoamine hypothesis of depression, there is evidence that alterations in neuronal plasticity in the hippocampus and other brain areas are critically involved in the pathophysiology of mood disorders.Materials and MethodsWestern blot (WB) and immunohistochemistry were used to investigate the basal immunochemical occurrence of brain‐derived neurotrophic factor (BDNF) and its high‐affinity tyrosine‐kinase receptor trkB in the dorsal and ventral hippocampus of adult RHA and RLA rats.Results WB analysis indicated that the optical density of BDNF‐ and trkB‐positive bands in the dorsal hippocampus is, respectively, 48% and 25% lower in RLA versus RHA rats. Densitometric analysis of BDNF‐ and trkB‐like immunoreactivity (LI) in brain sections showed that BDNF‐LI is 24% to 34% lower in the different sectors of the Ammon's horn of RLA versus RHA rats, whereas line‐related differences are observed in the dentate gyrus (DG) only in the ventral hippocampus. As for trkB‐LI, significant differences are observed only in the dorsal hippocampus, where density is 23% lower in the DG of RLA versus RHA rats, while no differences across lines occur in the Ammon's horn.ConclusionThese findings support the hypothesis that a reduced BDNF/trkB signaling in the hippocampus of RLA versus RHA rats may contribute to their more pronounced vulnerability to stress‐induced depression.

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“…This factor has been found diminished in the rat hippocampus after acute and chronic stress (Smith et al, 1995;Scaccianoce et al, 2003) and has proved to possess antidepressant action in different models of depression (Shirayama et al, 2002). Moreover, chronic treatment with FLX promotes BDNF expression in the rat hippocampus (De Foubert et al, 2004) that in turn leads to activation of genes and biochemical pathways involved in plasticity and survival (Mattson et al, 2004). At synaptic structural level, adult BDNF knockout mice show reduced number of vesicles docked at presynaptic active zones and marked decreased levels of SYN and synaptobrevin (Pozzo-Miller et al, 1999), alterations that can be reversed by BDNF administration (Pozzo-Miller et al, 1999), and somewhat resemble the synaptic protein decrease we observed in LH animals.…”

Section: Flx-induced Synaptic Remodeling and Behavioral Responsementioning

confidence: 99%

Maintenance Treatment with Fluoxetine is Necessary to Sustain Normal Levels of Synaptic Markers in an Experimental Model of Depression: Correlation with Behavioral Response

Reinés

Cereseto

Ferrero

et al. 2007

Neuropsychopharmacol

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Dysfunction of hippocampal plasticity has been proposed to play a critical role in the pathophysiology of depression. However, antidepressant drug effects on synaptic plasticity and cytoskeletal remodeling remain controversial. The aim of the present study was to evaluate in animals exposed to the learned helplessness (LH) paradigm, an accepted experimental model of depression, the effect of chronic treatment with fluoxetine (FLX) on synaptic and cytoskeletal proteins known to undergo plastic changes. Synaptophysin (SYN), postsynaptic density 95 (PSD-95), axon growth-associated protein 43 (GAP-43), and cytoskeletal proteins (intermediate neurofilaments and MAP-2) were studied in the hippocampus by immunohistochemistry. Whereas LH animals treated 21 days with saline (LH-S group) displayed diminished SYN and PSD-95 immunostainings in the CA3 but not in the DG, chronic treatment with FLX not only reversed the despaired behavior induced by exposure to LH paradigm, but also fully recovered SYN and PSD-95 labeling to control values. Similar results were obtained for the axonal remodeling marker GAP-43. FLX treatment did not modify either the decreased light neurofilament subunit (NFL) observed in the hippocampus of LH animals or any other cytoskeletal protein studied. When FLX treatment was withdrawn for 90 days in those LH-FLX animals in which reversion of despair had been observed at day 25, recurrence of despaired behavior was found accompanied by decreased SYN, PSD-95, and NFL labelings. Results indicate that the synapse remodeling induced by FLX in the CA3 region could underlie its behavioral efficacy despite the absence of cytoskeletal remodeling and that the stability of synaptic changes would depend on the continuous administration of the drug.

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Fluoxetine-induced change in rat brain expression of brain-derived neurotrophic factor varies depending on length of treatment

Cited by 227 publications

References 34 publications

Metabotropic Glutamate Receptor Subtype 7 Ablation Causes Dysregulation of the HPA Axis and Increases Hippocampal BDNF Protein Levels: Implications for Stress-Related Psychiatric Disorders

Metabotropic Glutamate Receptor Subtype 7 Ablation Causes Dysregulation of the HPA Axis and Increases Hippocampal BDNF Protein Levels: Implications for Stress-Related Psychiatric Disorders

Expression of BDNF and trkB in the hippocampus of a rat genetic model of vulnerability (Roman low‐avoidance) and resistance (Roman high‐avoidance) to stress‐induced depression

Maintenance Treatment with Fluoxetine is Necessary to Sustain Normal Levels of Synaptic Markers in an Experimental Model of Depression: Correlation with Behavioral Response

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