Diazepam induces FGF-2 mRNA in the hippocampus and striatum

Gómez‐Pinilla, Fernando; Dao, Lan; Choi, Jor-Shan; Ryba, Eeke.A

doi:10.1016/s0361-9230(00)00342-7

Cited by 22 publications

(13 citation statements)

References 54 publications

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“…Rats who received low maternal care have low levels of hippocampal FGF2 (Bredy et al, 2003) and exhibit high anxiety (Caldji et al, 1998). Most interestingly, treatment with anxiolytic drugs increase FGF2 expression in hippocampus (Gomez-Pinilla et al, 2000, Mallei et al, 2002). We therefore propose that FGF2 may be a key integrator of many influences, be they genetic, environmental or pharmacological, which define the propensity for anxiety behavior, with higher levels of FGF2 being consistently protective.…”

Section: Discussionmentioning

confidence: 99%

A New Role for FGF2 as an Endogenous Inhibitor of Anxiety

Pérez¹,

Clinton²,

Turner³

et al. 2009

J. Neurosci.

136

172

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Human postmortem studies have demonstrated that fibroblast growth factor-2 (FGF2) expression is decreased in the brain of depressed individuals. It remained unclear, however, whether this is a consequence of the illness or whether FGF2 plays a primary role in the control of mood and emotions. In this series of studies, we first ask whether endogenous FGF2 expression correlates with spontaneous anxiety, a trait associated with vulnerability to severe mood disorders in humans. This is tested in two genetically distinct groups of rats selectively bred to differ dramatically in their response to novelty and anxiety-provoking conditions (HRs ϭ low anxiety/high response to novelty vs LRs ϭ high anxiety/low response to novelty). We demonstrate that high-anxiety LRs have significantly lower levels of hippocampal FGF2 mRNA relative to low-anxiety HRs. We then demonstrate that FGF2 expression is modifiable by environmental factors that alter anxiety-thus, environmental complexity reduces anxiety behavior and induces FGF2 expression in hippocampus, particularly in highanxiety LRs. Finally, we directly test the role of FGF2 as an anxiolytic and show that a 3 week treatment regimen of peripherally administered FGF2 is highly effective at blunting anxiety behavior, specifically in high-anxiety LRs. This treatment is accompanied by an increase in survival of adult-born hippocampal cells, both neurons and astrocytes, most clearly in LRs. These findings implicate hippocampal FGF2 as a central integrator of genetic and environmental factors that modify anxiety, point to hippocampal neurogenesis and gliogenesis as key in this modulation, and underscore FGF2's potential as a new target for treatment of depression and anxiety disorders.

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Section: Discussionmentioning

confidence: 99%

A New Role for FGF2 as an Endogenous Inhibitor of Anxiety

Pérez¹,

Clinton²,

Turner³

et al. 2009

J. Neurosci.

136

172

View full text Add to dashboard Cite

show abstract

“…Limited FGF-2 down-regulation was apparent in those patients that had been treated with antidepressants (Evans et al, 2004), a finding also seen in mice in which antidepressants increased FGF-2 expression and immunoreactivity in hippocampus and PFC (Gómez-Pinilla et al, 2000; Maragnoli et al, 2004; Bachis et al, 2008; Elsayed et al, 2012). Furthermore, blockade of FGF-2 receptor signaling (Elsayed et al, 2012) or genetic knockout of FGF-2 (Jarosik et al, 2011) antagonized the behavioral effects of antidepressants in rodent models of depression, suggesting that this growth factor may be necessary for antidepressant effects to occur.…”

Section: Contribution Of Additional Growth Factors To Depression: Beymentioning

confidence: 96%

Interplay between pro-inflammatory cytokines and growth factors in depressive illnesses

Audet¹,

Anisman²

2013

Front. Cell. Neurosci.

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The development of depressive disorders had long been attributed to monoamine variations, and pharmacological treatment strategies likewise focused on methods of altering monoamine availability. However, the limited success achieved by treatments that altered these processes spurred the search for alternative mechanisms and treatments. Here we provide a brief overview concerning a possible role for pro-inflammatory cytokines and growth factors in major depression, as well as the possibility of targeting these factors in treating this disorder. The data suggest that focusing on one or another cytokine or growth factor might be counterproductive, especially as these factors may act sequentially or in parallel in affecting depressive disorders. It is also suggested that cytokines and growth factors might be useful biomarkers for individualized treatments of depressive illnesses.

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“…Thus, chronic antidepressant treatment for three weeks resulted in an increase in FGF2 24h later (Mallei et al, 2002). Similarly, FGF2 was increased (six and 12 hours) following acute treatment with an anxiolytic (Gomez-Pinilla et al, 2000). This led to the suggestion that FGF2, like BDNF, may mediate the actions of these drugs, and was consistent with the observation that patients on antidepressants expressed a lower degree of dysregulation in their FGF system relative to untreated MDD's.…”

Section: Affective Functions Of the Fgf Systemmentioning

confidence: 99%

The Fibroblast Growth Factor Family: Neuromodulation of Affective Behavior

Turner

Watson

Akil

2012

Neuron

140

126

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In this review we propose a broader view of the role of the fibroblast growth factor (FGF) family in modulating brain function. We suggest that some of the FGF ligands together with the FGF receptors are altered in individuals with affective disorder and modulate emotionality in animal models. Thus, we propose that members of the FGF family may be genetic predisposing factors for anxiety, depression or substance abuse; that they play a key organizing role during early development but continue to play a central role in neuroplasticity in adulthood; and that they work not only over extended time frames, but also via rapid signaling mechanisms, allowing them to exert an “on-line” influence on behavior. Therefore, the FGF family appears to be a prototype of “switch genes” that are endowed with organizational and modulatory properties across the lifespan, and that may represent molecular candidates as biomarkers and treatment targets for affective and addictive disorders.

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Diazepam induces FGF-2 mRNA in the hippocampus and striatum

Cited by 22 publications

References 54 publications

A New Role for FGF2 as an Endogenous Inhibitor of Anxiety

A New Role for FGF2 as an Endogenous Inhibitor of Anxiety

Interplay between pro-inflammatory cytokines and growth factors in depressive illnesses

The Fibroblast Growth Factor Family: Neuromodulation of Affective Behavior

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