Requirement of AQP4 for Antidepressive Efficiency of Fluoxetine: Implication in Adult Hippocampal Neurogenesis

Kong, Hui; Sha, Luolin; Fan, Yi; Xiao, Ming; Ding, Jingzhong; Wu, Jie; Hu, Gang

doi:10.1038/npp.2008.185

Cited by 98 publications

(76 citation statements)

References 71 publications

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“…As previously reported [17,21] , there is no difference in basal hippocampal neurogenesis between AQP4 KO and wild-type mice, although AQP4 deficiency impairs the proliferation and migration of aNSC in our culture conditions [10] . This discordance between in vivo and in vitro was firstly observed in a mouse model of depression 316 following fluoxetine infusion [17] and then confirmed in long-term training of spatial learning and memory [21] .…”

Section: Discussionsupporting

confidence: 57%

“…Briefly, the mice (6 per group) were given BrdU intraperitoneally (4 × 50 mg/kg every 2 h; Sigma-Aldrich, St. Louis, MO, USA) 3 h after LPS stimuli and then sacrificed 24 h after the first BrdU injection. BrdU-positive cells were labeled and analyzed as in our previous study [17] .…”

Section: Bromodeoxyuridine Incorporationmentioning

confidence: 99%

“…Bromodeoxyuridine (BrdU) incorporation was calculated as described previously [17] . Briefly, the mice (6 per group) were given BrdU intraperitoneally (4 × 50 mg/kg every 2 h; Sigma-Aldrich, St. Louis, MO, USA) 3 h after LPS stimuli and then sacrificed 24 h after the first BrdU injection.…”

Section: Bromodeoxyuridine Incorporationmentioning

confidence: 99%

“…The numbers of BrdU-positive and GFAP-positive cells were measured using an Optical Fractionator with Stereo Investigator software (Microbrightfield, USA) as described previously [17] . The boundaries of the DG and subgranular layer formation were demarcated for stereological analysis using a low-power (×4) magnification lens.…”

Section: Quantitation Of Immunohistochemistrymentioning

confidence: 99%

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Aquaporin-4 Mediates the Suppressive Effect of Lipopolysaccharide on Hippocampal Neurogenesis

Liang

Yong

Huang

et al. 2016

Neuroimmunomodulation

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Objective: Aquaporin-4 (AQP4), a key molecule for water homeostasis in the brain, is associated with adult neurogenesis, but its mechanisms regulating adult neural stem cells (aNSC) remain largely unexplored. Neuroinflammation has a relevant influence on adult neurogenesis, which is a common feature in various neurodegenerative diseases. Considering the possible link between neuroinflammation and AQP4, we speculate that AQP4 may mediate the synthesis and release of proinflammatory cytokines in glia and then indirectly regulate adult hippocampal neurogenesis. Methods: Using AQP4 knockout mice, we investigated the effects of AQP4 on hippocampal neurogenesis after lipopolysaccharide (LPS)-induced neuroinflammation. Results: We unexpectedly found that AQP4 deficiency attenuated the decrease in aNSC proliferation after systemic LPS exposure, accompanied by inhibition of glial activation and suppression of the production of proinflammatory cytokines in the hippocampus. Meanwhile, in vivo studies demonstrated that LPS-induced activated microglia did not express AQP4, indicating the impossibility of direct regulation of AQP4 to activate microglia. Furthermore, we demonstrated in vitro that AQP4 deficiency inhibited astrocyte activation and reduced the release of proinflammatory cytokines from astrocytes. Conclusion: Our data suggest that AQP4 mediates the suppressive effect of neuroinflammation on hippocampal neurogenesis via regulation of the astroglial response.

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Section: Discussionsupporting

confidence: 57%

Section: Bromodeoxyuridine Incorporationmentioning

confidence: 99%

Section: Bromodeoxyuridine Incorporationmentioning

confidence: 99%

Section: Quantitation Of Immunohistochemistrymentioning

confidence: 99%

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Aquaporin-4 Mediates the Suppressive Effect of Lipopolysaccharide on Hippocampal Neurogenesis

Liang

Yong

Huang

et al. 2016

Neuroimmunomodulation

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“…Aquaporin-4 (AQP4), a predominant water channel in adult brain, is widely expressed in astrocytes (Nielsen et al, 1997) and plays important roles in the regulation of extravascular brain water, brain volume homeostasis, and cerebrospinal fluid production (AmiryMoghaddam and Ottersen, 2003). A lot of evidence shows that AQP4 is involved in the pathophysiology of cerebral disorders, including stroke, cerebral edema, traumatic brain injury, Parkinson's disease, epilepsy, and depression, and so on (Binder et al, 2006;Chi et al, 2011;Ding et al, 2009;Friedman et al, 2009;Kong et al, 2009;Thrane et al, 2011). Recent studies demonstrate that AQP4 knockout (KO) inhibits the formation of glial cell-derived neurotrophic factor and increases microglial inflammatory responses in MPTP-treated mouse model of Parkinson's disease (Chi et al, 2011;Fan et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Aquaporin-4 Deficiency Impairs Synaptic Plasticity and Associative Fear Memory in the Lateral Amygdala: Involvement of Downregulation of Glutamate Transporter-1 Expression

Wang

et al. 2012

Neuropsychopharmacol

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105

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Astrocytes are implicated in information processing, signal transmission, and regulation of synaptic plasticity. Aquaporin-4 (AQP4) is the major water channel in adult brain and is primarily expressed in astrocytes. A growing body of evidence indicates that AQP4 is a potential molecular target for the regulation of astrocytic function. However, little is known about the role of AQP4 in synaptic plasticity in the amygdala. Therefore, we evaluated long-term potentiation (LTP) in the lateral amygdala (LA) and associative fear memory of AQP4 knockout (KO) and wild-type mice. We found that AQP4 deficiency impaired LTP in the thalamo-LA pathway and associative fear memory. Furthermore, AQP4 deficiency significantly downregulated glutamate transporter-1 (GLT-1) expression and selectively increased NMDA receptor (NMDAR)-mediated EPSCs in the LA. However, low concentration of NMDAR antagonist reversed the impairment of LTP in KO mice. Upregulating GLT-1 expression by chronic treatment with ceftriaxone also reversed the impairment of LTP and fear memory in KO mice. These findings imply a role for AQP4 in synaptic plasticity and associative fear memory in the amygdala by regulating GLT-1 expression.

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Roles of Ion Transport in Control of Cell Motility

Stock

Ludwig

Hanley

et al. 2013

Comprehensive Physiology

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Cell motility is an essential feature of life. It is essential for reproduction, propagation, embryonic development, and healing processes such as wound closure and a successful immune defense. If out of control, cell motility can become life-threatening as, for example, in metastasis or autoimmune diseases. Regardless of whether ciliary/flagellar or amoeboid movement, controlled motility always requires a concerted action of ion channels and transporters, cytoskeletal elements, and signaling cascades. Ion transport across the plasma membrane contributes to cell motility by affecting the membrane potential and voltage-sensitive ion channels, by inducing local volume changes with the help of aquaporins and by modulating cytosolic Ca(2+) and H(+) concentrations. Voltage-sensitive ion channels serve as voltage detectors in electric fields thus enabling galvanotaxis; local swelling facilitates the outgrowth of protrusions at the leading edge while local shrinkage accompanies the retraction of the cell rear; the cytosolic Ca(2+) concentration exerts its main effect on cytoskeletal dynamics via motor proteins such as myosin or dynein; and both, the intracellular and the extracellular H(+) concentration modulate cell migration and adhesion by tuning the activity of enzymes and signaling molecules in the cytosol as well as the activation state of adhesion molecules at the cell surface. In addition to the actual process of ion transport, both, channels and transporters contribute to cell migration by being part of focal adhesion complexes and/or physically interacting with components of the cytoskeleton. The present article provides an overview of how the numerous ion-transport mechanisms contribute to the various modes of cell motility.

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Requirement of AQP4 for Antidepressive Efficiency of Fluoxetine: Implication in Adult Hippocampal Neurogenesis

Cited by 98 publications

References 71 publications

Aquaporin-4 Mediates the Suppressive Effect of Lipopolysaccharide on Hippocampal Neurogenesis

Aquaporin-4 Mediates the Suppressive Effect of Lipopolysaccharide on Hippocampal Neurogenesis

Aquaporin-4 Deficiency Impairs Synaptic Plasticity and Associative Fear Memory in the Lateral Amygdala: Involvement of Downregulation of Glutamate Transporter-1 Expression

Roles of Ion Transport in Control of Cell Motility

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