Corticosterone acutely prolonged <i>N</i>‐methyl‐<scp>d</scp>‐aspartate receptor‐mediated Ca<sup>2+</sup> elevation in cultured rat hippocampal neurons

Takahashi, Takehiro; Kimoto, Tsunenobu; Tanabe, Nari; Hattori, Takaaki; Yasumatsu, Nobuaki; Kawato, Suguru

doi:10.1046/j.1471-4159.2002.01251.x

Cited by 160 publications

(101 citation statements)

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“…Expanding the scope of previous reports on CORT activation of PKA and PKC, with subsequent alterations of NMDA receptor trafficking and integration into the postsynaptic density (3,5), our study shows that recruitment of downstream signaling molecules depends on the simultaneous activation of PKC, Akt/PKB, and PKA. Given that the synaptic actions of many neurotransmitters and neuromodulators occur through activation of PKA, Akt/PKB, and PKC (for example, see Ref.…”

Section: Discussionsupporting

confidence: 73%

“…Because plasticity-inducing stimuli are known to regulate cell surface availability of NMDAR through Pyk2 and its SFK-dependent amplification loop (21,61,62), we here monitored synaptic NMDAR surface localization in CORT-treated hippocampal neurons. Our results show concomitant increases in the phosphorylation of the Tyr-1472 residue in the cytoplasmic tail of the NR2B subunit of the NMDAR and surface retention of NMDAR after CORT application, providing a molecular explanation for the induction of fast CORT- induced changes in NMDAR-induced Ca 2ϩ currents (5). Previous studies showed that the cytoplasmic tail of the NR2 subunit is a major target of TK, with the Tyr-1472 residue appearing to be a major regulator of NMDAR endocytosis as it provides the binding site for the endocytic adaptor AP-2 (35,36).…”

Section: Discussionmentioning

confidence: 57%

“…Glucocorticoids (GCs) 5 are essential for immediate and long term behavioral and physiological adaptations to stress. Generally, the adaptations triggered by GC secretion are considered to result from activation of glucocorticoid (GR) and/or mineralocorticoid (MR) receptors, ligand-activated transcription factors (or nuclear receptors) that regulate gene expression.…”

mentioning

confidence: 99%

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Non-receptor-tyrosine Kinases Integrate Fast Glucocorticoid Signaling in Hippocampal Neurons

Yang

Roselli

Patchev

et al. 2013

Journal of Biological Chemistry

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Background: The intracellular signaling cascades through which corticosterone rapidly alters neuronal activity are poorly defined. Results: Corticosterone alters glutamatergic transmission by activating diverse GPCR-dependent signaling pathways. Conclusion: Corticosterone-induced changes in neuronal excitability are initiated at the plasma membrane. Significance: The sequential recruitment and integration of diverse signaling cascades by corticosterone adds to the understanding of how steroids rapidly alter neuronal function.

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Section: Discussionsupporting

confidence: 73%

Section: Discussionmentioning

confidence: 57%

mentioning

confidence: 99%

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Non-receptor-tyrosine Kinases Integrate Fast Glucocorticoid Signaling in Hippocampal Neurons

Yang

Roselli

Patchev

et al. 2013

Journal of Biological Chemistry

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“…Such an overstimulation of the NMDA receptor results in excitotoxic neuronal damage. 165 Nair and Bonneau 166 could demonstrate that restraint-induced psychological stress stimulates proliferation of microglia, which was prevented by blockade of corticosterone synthesis, the GR or the NMDA receptor. These data show that stress-induced microglia proliferation is mediated by corticosterone-induced, NMDA receptor-mediated activation within the CNS.…”

Section: Stress and Cns Immune Systemmentioning

confidence: 99%

The immune-mediated alteration of serotonin and glutamate: towards an integrated view of depression

2007

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Beside the well-known deficiency in serotonergic neurotransmission as pathophysiological correlate of major depression (MD), recent evidence points to a pivotal role of increased glutamate receptor activation as well. However, cause and interaction of these neurotransmitter alterations are not understood. In this review, we present a hypothesis integrating current concepts of neurotransmission and hypothalamus-pituitary-adrenal (HPA) axis dysregulation with findings on immunological alterations and alterations in brain morphology in MD. An immune activation including increased production of proinflammatory cytokines has repeatedly been described in MD. Proinflammatory cytokines such as interleukin-2, interferon-c, or tumor necrosis factor-a activate the tryptophan-and serotonin-degrading enzyme indoleamine 2,3-dioxygenase (IDO). Depressive states during inflammatory somatic disorders are also associated with increased proinflammatory cytokines and increased consumption of tryptophan via activation of IDO. An enhanced consumption of serotonin and its precursor tryptophan through IDO activation could well explain the reduced availability of serotonergic neurotransmission in MD. An increased activation of IDO and its subsequent enzyme kynurenine monooxygenase by proinflammatory cytokines, moreover, leads to an enhanced production of quinolinic acid, a strong agonist of the glutamatergic N-methyl-D-aspartate receptor. In inflammatory states of the central nervous system, IDO is mainly activated in microglial cells, which preferentially metabolize tryptophan to the NMDA receptor agonist quinolinic acid, whereas astrocytes -counteracting this metabolism due to the lack of an enzyme of this metabolism -have been observed to be reduced in MD. Therefore the type 1/type 2 immune response imbalance, associated with an astrocyte/microglia imbalance, leads to serotonergic deficiency and glutamatergic overproduction. Astrocytes are further strongly involved in re-uptake and metabolic conversion of glutamate. The reduced number of astrocytes could contribute to both, a diminished counterregulation of IDO activity in microglia and an altered glutamatergic neurotransmission. Further search for antidepressant agents should take into account anti-inflammatory drugs, for example, cyclooxygenase-2 inhibitors, might exert antidepressant effects by acting on serotonergic deficiency, glutamatergic hyperfunction and antagonizing neurotoxic effects of quinolinic acid. Molecular Psychiatry (2007) 12, 988-1000; doi:10.1038/sj.mp.4002006; published online 24 April 2007 Keywords: major depression; psychoneuroimmunology; IDO; glutamate; immune system; serotonin Glutamate in depressionGlutamatergic neurotransmission is involved in depression and interacts with the serotonergic and noradrenergic systems The common therapeutic mechanism of antidepressant drugs is the enhancement of serotonergic and/or noradrenergic neurotransmission. On the basis of this pharmacological profile of antidepressant drugs, neurochemical research on major depression ...

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“…A previous study showed that corticosterone could facilitate the Ca 2+ influx through the voltage-dependent calcium channels in cultured hippocampal neurons [99]. A recent study also showed that corticosterone acutely prolonged NMDA-induced Ca 2+ elevation in cultured hippocampal neurons [100]. These different responses of the rapid non-genomic effects to glucocorticoids suggest the involvement of different receptors and cellular signaling pathways in each cell type.…”

Section: Effects Of Glucocorticoids On the Atp-induced No And Ca 2+ Smentioning

confidence: 99%

Role of nitric oxide on purinergic signalling in the cochlea

Harada

2010

Purinergic Signalling

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In the inner ear, there is considerable evidence that extracellular adenosine 5′-triphosphate (ATP) plays an important role in auditory neurotransmission as a neurotransmitter or a neuromodulator, although the potential role of adenosine signalling in the modulation of auditory neurotransmission has also been reported. The activation of ligand-gated ionotropic P2X receptors and G proteincoupled metabotropic P2Y receptors has been reported to induce an increase of intracellular Ca 2+ concentration ([Ca 2+ ] i ) in inner hair cells (IHCs), outer hair cells (OHCs), spiral ganglion neurons (SGNs), and supporting cells in the cochlea. ATP may participate in auditory neurotransmission by modulating [Ca 2+ ] i in the cochlear cells. Recent studies showed that extracellular ATP induced nitric oxide (NO) production in IHCs, OHCs, and SGNs, which affects the ATP-induced Ca 2+ response via the NO-cGMP-PKG pathway in those cells by a feedback mechanism. A cross-talk between NO and ATP may therefore exist in the auditory signal transduction. In the present article, I review the role of NO on the ATP-induced Ca 2+ signalling in IHCs and OHCs. I also consider the possible role of NO in the ATP-induced Ca 2+ signalling in SGNs and supporting cells.

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Corticosterone acutely prolonged N‐methyl‐d‐aspartate receptor‐mediated Ca²⁺ elevation in cultured rat hippocampal neurons

Cited by 160 publications

References 56 publications

Non-receptor-tyrosine Kinases Integrate Fast Glucocorticoid Signaling in Hippocampal Neurons

Non-receptor-tyrosine Kinases Integrate Fast Glucocorticoid Signaling in Hippocampal Neurons

The immune-mediated alteration of serotonin and glutamate: towards an integrated view of depression

Role of nitric oxide on purinergic signalling in the cochlea

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Corticosterone acutely prolonged N‐methyl‐d‐aspartate receptor‐mediated Ca2+ elevation in cultured rat hippocampal neurons

Cited by 160 publications

References 56 publications

Non-receptor-tyrosine Kinases Integrate Fast Glucocorticoid Signaling in Hippocampal Neurons

Non-receptor-tyrosine Kinases Integrate Fast Glucocorticoid Signaling in Hippocampal Neurons

The immune-mediated alteration of serotonin and glutamate: towards an integrated view of depression

Role of nitric oxide on purinergic signalling in the cochlea

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Product

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Corticosterone acutely prolonged N‐methyl‐d‐aspartate receptor‐mediated Ca²⁺ elevation in cultured rat hippocampal neurons