Lithium blocks stress-induced changes in depressive-like behavior and hippocampal cell fate: The role of glycogen-synthase-kinase-3β

Silva, Raian; Mesquita, Ana; Bessa, João M.; Sousa, João Carlos; Sotiropoulos, Ioannis; Leão, Pedro; Almeida, Osborne F. X.; Sousa, Nuno

doi:10.1016/j.neuroscience.2007.12.026

Cited by 151 publications

(111 citation statements)

References 63 publications

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“…Furthermore, inhibition of GSK3b by phosphorylation following lithiuminduced AKT activation has been shown to exert antiapoptotic effects (Jope and Bijur, 2002). These results are consistent with the neurotrophic-neuroprotective effects of mood stabilizers and antidepressants thought, at least partially, to be mediated by inhibition of GSK3b (Manji et al, 2003;Silva et al, 2008). Furthermore, indirect (upstream) regulation of GSK3 constitutes a new target for the control of affective disorders and highlights the role of neuroplasticity in their induction and treatment (Mathew et al, 2008;Jope and Roh, 2006;O'Brien and Klein, 2007;McClung and Nestler, 2008).…”

Section: Adult Neurogenesis and Antidepressantsupporting

confidence: 64%

“…We also showed that agomelatine increases the phosphorylation of ERK1/2, AKT, and GSK3b known to transduce the effects of antidepressant agent and mood stabilizers on proliferation of hippocampal neural progenitors (Jiang et al, 2005;Wexler et al, 2008;Silva et al, 2008). The enhanced survival of new granule cells may also be related to the activation of MAPK (ERK1/2) and PI-3K signaling pathways, as previously shown in vitro (Almeida et al, 2005), and hippocampal NSCs can be protected from apoptosis by antidepressant-induced activation of BDNF and the MAPK pathway (Peng et al, 2008).…”

Section: Adult Neurogenesis and Antidepressantmentioning

confidence: 66%

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Mechanisms Contributing to the Phase-Dependent Regulation of Neurogenesis by the Novel Antidepressant, Agomelatine, in the Adult Rat Hippocampus

Soumier¹,

Banasr²,

Lortet³

et al. 2009

Neuropsychopharmacol

145

138

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Agomelatine is a novel antidepressant acting as a melatonergic receptor agonist and serotonergic (5-HT 2C ) receptor antagonist. In adult rats, chronic agomelatine treatment enhanced cell proliferation and neurogenesis in the ventral hippocampus (VH), a region pertinent to mood disorders. This study compared the effects of agomelatine on cell proliferation, maturation, and survival and investigated the cellular mechanisms underlying these effects. Agomelatine increased the ratio of mature vs immature neurons and enhanced neurite outgrowth of granular cells, suggesting an acceleration of maturation. The influence of agomelatine on maturation and survival was accompanied by a selective increase in the levels of BDNF (brain-derived neurotrophic factor) vs those of VEGF (vascular endothelial factor) and IGF-1 (insulin-like growth factor 1), which were not affected. Agomelatine also activated several cellular signals (extracellular signal-regulated kinase1/2, protein kinase B, and glycogen synthase kinase 3b) known to be modulated by antidepressants and implicated in the control of proliferation/survival. Furthermore, as agomelatine possesses both melatonergic agonist and serotonergic (5-HT 2C ) antagonist properties, we determined whether melatonin and 5-HT 2C receptor antagonists similarly influence cell proliferation and survival. Only the 5-HT 2C receptor antagonists, SB243,213 or S32006, but not melatonin, mimicked the effects of agomelatine on cell proliferation in VH. The promoting effect of agomelatine on survival was not reproduced by the 5-HT 2C receptor antagonists or melatonin alone. However, it was blocked by a melatonin antagonist, S22153. These results show that agomelatine treatment facilitates all stages of neurogenesis and suggest that a joint effect of melatonin agonism and 5HT 2C antagonism may be involved in promotion by agomelatine of survival in the hippocampus.

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Section: Adult Neurogenesis and Antidepressantsupporting

confidence: 64%

Section: Adult Neurogenesis and Antidepressantmentioning

confidence: 66%

Mechanisms Contributing to the Phase-Dependent Regulation of Neurogenesis by the Novel Antidepressant, Agomelatine, in the Adult Rat Hippocampus

Soumier¹,

Banasr²,

Lortet³

et al. 2009

Neuropsychopharmacol

145

138

View full text Add to dashboard Cite

show abstract

“…Finally, the prevailing perception in the literature, suggests FST to be a proper test to show neurogenesis-dependence of antidepressant efficacy. Several groups described X-irradiation to block antidepressant effects using FST (e.g., Zhu et al, 2010;Garza et al, 2012) while correlative observations linking antidepressant treatment effects in FST and adult hippocampal neurogenesis have been reported numerous times (Liu et al, 2008;Silva et al, 2008;Schmidt and Duman, 2010;Wainwright et al, 2011;Wang et al, 2011;Jiang et al, 2012;Lin and Wang, 2014;Lu et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Mice with ablated adult brain neurogenesis are not impaired in antidepressant response to chronic fluoxetine

Jedynak

Kos

Sandi

et al. 2014

Journal of Psychiatric Research

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a b s t r a c tThe neurogenesis hypothesis of major depression has two main facets. One states that the illness results from decreased neurogenesis while the other claims that the very functioning of antidepressants depends on increased neurogenesis. In order to verify the latter, we have used cyclin D2 knockout mice (cD2 KO mice), known to have virtually no adult brain neurogenesis, and we demonstrate that these mice successfully respond to chronic fluoxetine. After unpredictable chronic mild stress, mutant mice showed depression-like behavior in forced swim test, which was eliminated with chronic fluoxetine treatment, despite its lack of impact on adult hippocampal neurogenesis in cD2 KO mice. Our results suggest that new neurons are not indispensable for the action of antidepressants such as fluoxetine. Using forced swim test and tail suspension test, we also did not observe depression-like behavior in control cD2 KO mice, which argues against the link between decreased adult brain neurogenesis and major depression.

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“…Moreover, recent reports have described that Li and VPA affect neurogenesis through increasing cell proliferation and/or promotion of neuronal differentiation of neural precursor cells (Chen et al, 2000;Son et al, 2003;Hao et al, 2004;Hsieh et al, 2004;Kim JS et al, 2004;Laeng et al, 2004;Wexler et al, 2008) and that Li blocks the effects of stress on depression-like behaviors through increasing hippocampal neurogenesis in adult rodent models (Silva et al, 2008). Results of these studies suggest that adult hippocampal neurogenesis plays an important role in the therapeutic action of mood stabilizers as well.…”

Section: Introductionmentioning

confidence: 92%

“…Adult neurogenesis in DG is decreased in rodent models for stress-related disorders (Malberg and Duman, 2003;Jayatissa et al, 2006;Silva et al, 2008). Although it remains unclear how adult neurogenesis in DG is decreased in these models, reports of some studies have suggested that glucocorticoids are involved in them (Cameron and McKay, 1999;Kim JB et al, 2004).…”

Section: Effects Of Mood Stabilizers On Adp Proliferationmentioning

confidence: 99%

Effects of mood stabilizers on adult dentate gyrus-derived neural precursor cells

Boku¹,

Nakagawa²,

Masuda³

et al. 2011

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Neurogenesis in the adult dentate gyrus (DG) is considered to be partly involved in the action of mood stabilizers. However, it remains unclear how mood stabilizers affect neural precursor cells in adult DG. We have established a culture system of adult rat DG-derived neural precursor cells (ADP) and have shown that lithium, a mood stabilizer, and dexamethasone, an agonist of glucocorticoid receptor, reciprocally regulate ADP proliferation. Neurogenesis constitutes not only proliferation of neural precursor cells but also apoptosis and differentiation. To develop further understanding of mood stabilizer effects on neural precursor cells in adult DG, we investigated and compared the effects of four common mood stabilizers--lithium, valproate, carbamazepine, and lamotrigine--on ADP proliferation, apoptosis, and differentiation. ADP proliferation, decreased by dexamethasone, was examined using Alamar Blue assay. Using TUNEL assay, ADP apoptosis induced by staurosporine was examined. The differentiated ADP induced by retinoic acid was characterized by immunostaining with anti-GFAP or anti-Tuj1 antibody. Lithium and valproate, but not carbamazepine and lamotrigine, recovered ADP proliferation decreased by dexamethasone. All four mood stabilizers decreased ADP apoptosis.Retinoic acid differentiated ADP into both neurons and astrocytes. Lithium and carbamazepine increased the ratio of neurons and decreased that of astrocytes. However, valproate and lamotrigine increased the ratio of astrocytes and decreased that of neurons. Therefore, these four stabilizers exhibited both common and differential effects on ADP proliferation, apoptosis, and differentiation.

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Lithium blocks stress-induced changes in depressive-like behavior and hippocampal cell fate: The role of glycogen-synthase-kinase-3β

Cited by 151 publications

References 63 publications

Mechanisms Contributing to the Phase-Dependent Regulation of Neurogenesis by the Novel Antidepressant, Agomelatine, in the Adult Rat Hippocampus

Mechanisms Contributing to the Phase-Dependent Regulation of Neurogenesis by the Novel Antidepressant, Agomelatine, in the Adult Rat Hippocampus

Mice with ablated adult brain neurogenesis are not impaired in antidepressant response to chronic fluoxetine

Effects of mood stabilizers on adult dentate gyrus-derived neural precursor cells

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