Enhancement of Hippocampal Neurogenesis by Lithium

Chen, Guang; Rajkowska, Grażyna; Du, Fuliang; Seraji‐Bozorgzad, Navid; Manji, Husseini K.

doi:10.1046/j.1471-4159.2000.0751729.x

Cited by 561 publications

(365 citation statements)

References 38 publications

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“…These results suggest that normal BDNF-TrkB signaling is requisite for the long-term survival of newborn neurons in the dentate gyrus (Sairanen et al, 2005). Importantly, antidepressants and the mood stabilizer lithium have been shown to elicit an increase in hippocampal neurogenesis (Chen et al, 2000;Malberg et al, 2000). This antidepressantinduced survival is lost in mice with impaired BDNF signaling (Sairanen et al, 2005).…”

Section: Bdnfmentioning

confidence: 97%

Interaction between BDNF and Serotonin: Role in Mood Disorders

Martinowich

2007

Neuropsychopharmacol

686

458

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Brain-derived neurotrophic factor (BDNF) and serotonin (5-hydroxytryptamine, 5-HT) are two seemingly distinct signaling systems that play regulatory roles in many neuronal functions including survival, neurogenesis, and synaptic plasticity. A common feature of the two systems is their ability to regulate the development and plasticity of neural circuits involved in mood disorders such as depression and anxiety. BDNF promotes the survival and differentiation of 5-HT neurons. Conversely, administration of antidepressant selective serotonin reuptake inhibitors (SSRIs) enhances BDNF gene expression. There is also evidence for synergism between the two systems in affective behaviors and genetic epitasis between BDNF and the serotonin transporter genes.

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Section: Bdnfmentioning

confidence: 97%

Interaction between BDNF and Serotonin: Role in Mood Disorders

Martinowich

2007

Neuropsychopharmacol

686

458

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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: 93%

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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“…Exposure to stress (which is used as an animal model of depression) is associated with a decrease in neurogenesis, while a deprived environment, which is used as a model of childhood neglect and is linked to depression, also results in a decrease in neurogenesis (Kempermann et al 1997;Kempermann et al 1998). This contrasts with antidepressant treatment or exercise (which has an anti-depressant effect (Blumenthal et al 1999)), which lead to an improvement in depression-like behaviors and an increase in neurogenesis (Chen et al 2000;Coyle and Duman 2003;D'Sa and Duman 2002;Duman 2004;Garcia 2002;Jacobs 2002;Kempermann 2002;Malberg et al 2000;Santarelli et al 2003;van Praag et al 1999). If 13-cis RA has the reverse effect to these antidepressants, reducing neurogenesis, this provides a plausible mechanism by which isotretinoin may contribute to depression.…”

Section: Ra and The Hippocampusmentioning

confidence: 99%

The neurobiology of retinoic acid in affective disorders

Bremner

McCaffery

2008

Progress in Neuro-Psychopharmacology and Biological Psychiatry

147

154

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Current models of affective disorders implicate alterations in norepinephrine, serotonin, dopamine, and CRF/cortisol; however treatments targeted at these neurotransmitters or hormones have led to imperfect resolution of symptoms, suggesting that the neurobiology of affective disorders is incompletely understood. Until now retinoids have not been considered as possible contributors to affective disorders. Retinoids represent a family of compounds derived from Vitamin A that perform a large number of functions, many via the vitamin A product, retinoic acid. This signaling molecule binds to specific retinoic acid receptors in the brain which, like the glucocorticoid and thyroid hormone receptors, are part of the nuclear receptor superfamily and regulate gene transcription. Research in the field of retinoic acid in the CNS has focused on the developing brain, in part stimulated by the observation that isotretinoin (13-cis retinoic acid), an isomer of retinoic acid used in the treatment of acne, is highly teratogenic for the CNS. More recent work has suggested that retinoic acid may influence the adult brain; animal studies indicated that the administration of isotretinoin is associated with alterations in behavior as well as inhibition of neurogenesis in the hippocampus. Clinical evidence for an association between retinoids and depression includes case reports in the literature, studies of health care databases, and other sources. A preliminary PET study in human subjects showed that isotretinoin was associated with a decrease in orbitofrontal metabolism. Several studies have shown that the molecular components required for retinoic acid signaling are expressed in the adult brain ; the overlap of brain areas implicated in retinoic acid function and stress and depression suggest that retinoids could play a role in affective disorders. This report reviews the evidence in this area and describes several systems that may be targets of retinoic acid and which contribute to the pathophysiology of depression.

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Enhancement of Hippocampal Neurogenesis by Lithium

Cited by 561 publications

References 38 publications

Interaction between BDNF and Serotonin: Role in Mood Disorders

Interaction between BDNF and Serotonin: Role in Mood Disorders

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

The neurobiology of retinoic acid in affective disorders

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