Stimulation of N-methyl-d-aspartate (NMDA) receptors inhibits neuronal migration in embryonic cerebral cortex: a tissue culture study

Kihara, Minako; Yoshioka, Hiroshi; Hirai, Kiyoshi; Hasegawa, Kou; Kizaki, Zenro; Sawada, Tadashi

doi:10.1016/s0165-3806(02)00490-x

Cited by 24 publications

(26 citation statements)

References 9 publications

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“…Here, we demonstrate that the transmitters involved in this paracrine nonsynaptic mode of communication may be responsible of the modulation of neuronal migration, thus confirming that paracrine transmitters influence brain construction. This study shed new light on the results of the numerous studies investigating the modulatory role played by the transmitters during CNS development (Komuro and Rakic, 1993;Behar et al, 1998Behar et al, , 1999Behar et al, , 2000Behar et al, , 2001Fueshko et al, 1998;Hirai et al, 1999;Bless et al, 2000;Simonian and Herbison, 2001;Kihara et al, 2002;Lopez-Bendito et al, 2003). As suggested by Owens and Kriegstein (2002), one could hypothesize that the modulation of neuronal migration by transmitters in those previous studies might be mediated exclusively by a nonvesicular release.…”

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confidence: 52%

“…Indeed, several studies that focused on various brain structures (cerebellar cortex, cerebral cortex, olfactory epithelium, basal forebrain) and neuronal subtypes (granule cells, cortical neuroblasts, tangentially migrating interneurons, luteinizing hormonereleasing hormone neuroblasts, gonadotropin-releasing hormone neuroblasts) have been performed using different protocols (dissociated cells in microchemotaxis chambers, slice preparation). These studies have led to the conclusion that transmitters, GABA and glutamate, acting on several receptor subtypes (GABA A , GABA B , GABA C , NMDA, AMPA) have a crucial modulatory effect on migrating neuroblasts, acting as motility-promoting signals (Behar et al, 1998(Behar et al, , 1999(Behar et al, , 2000(Behar et al, , 2001Hirai et al, 1999;Simonian and Herbison, 2001;Lopez-Bendito et al, 2003), acceleratory signals (Komuro and Rakic, 1993), or stop signals (Behar et al, 1998(Behar et al, , 2000Fueshko et al, 1998;Bless et al, 2000;Simonian and Herbison, 2001;Kihara et al, 2002). However, in contrast to these observations, there is no deficit in cortical layering and synapse formation in mice in which vesicular release has been deleted: munc18-1 mutant mice (Verhage et al, 2000) or munc13-1/2 double knock-out (KO) mice (Varoqueaux et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

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A Noncanonical Release of GABA and Glutamate Modulates Neuronal Migration

Manent

Demarque²,

Jorquera³

et al. 2005

J. Neurosci.

190

175

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Immature neurons express GABA and glutamate receptors before synapse formation, and both transmitters are released at an early developmental stage. We have now tested the hypothesis that the ongoing release of GABA and glutamate modulates neuronal migration. Using 5-bromo-2Ј-deoxyuridine labeling and cocultures of hippocampal slices obtained from naive and green fluorescent proteintransgenic mice, we report that migration is severely affected by GABA A or NMDA receptor antagonist treatments. These effects were also present in munc18-1 knock-out slices in which soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE)-dependent vesicular secretion of transmitters has been deleted. GABA A antagonists were more efficient than NMDA antagonists to reduce cell migration, in keeping with the earlier maturation of GABAergic mechanisms. We conclude that GABA and, to a lesser degree, glutamate released in a SNARE-independent mechanism exert a paracrine action on neuronal migration.

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confidence: 52%

Section: Introductionmentioning

confidence: 99%

A Noncanonical Release of GABA and Glutamate Modulates Neuronal Migration

Manent

Demarque²,

Jorquera³

et al. 2005

J. Neurosci.

190

175

View full text Add to dashboard Cite

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“…In addition, activation of NMDAR decreases basal actin polymerization state and TGF-␤1-induced actin reorganization in HK-2. The effect of NMDAR activation and Ca 2ϩ on cell migration 19,20 and actin organization 26,27 has previously been reported in different cell types. Nahm et al 20 showed that Ca 2ϩ entry through activated NMDAR inhibited keratinocyte outgrowth and migration.…”

Section: Discussionmentioning

confidence: 89%

“…Nahm et al 20 showed that Ca 2ϩ entry through activated NMDAR inhibited keratinocyte outgrowth and migration. Kihara et al 19 reported that stimulation of NMDAR inhibited neuronal migration in embryonic rat cerebral cortex. Furthermore, Cristofanilli and Akopian 27 showed that the NMDAR activation and influx of Ca 2ϩ caused a reduction of F-actin in retinal neurons of salamander, whereas NMDAR activation in rat cerebellar granule cells rapidly shifted F/G-actin equilibrium in favor of depolymerization.…”

Section: Discussionmentioning

confidence: 99%

“…Although the activity of calcium channels is important in the regulation of cell migration, 19 -22 calcium signaling is significant in mediating actin rearrangement 23,24 and organization of cadherins and catenins into intercellular junctions. 25 Indeed, NMDAR activation has been shown to induce changes in actin organization in cerebellar granule cells 26 and retinal neurons 27 and to inhibit cell migration in neurons 19 and keratinocytes. 20 Taking into consideration knowledge of multiple characteristics of NMDAR in a variety of tissues, including renal itself, we sought to examine its role in the maintenance of the epithelial phenotype of proximal tubular epithelial cells (PTECs) and in tubular EMT in vitro.…”

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confidence: 99%

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Glutamatergic Signaling Maintains the Epithelial Phenotype of Proximal Tubular Cells

Božić

Rooij

Parisi

et al. 2011

Journal of the American Society of Nephrology

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Epithelial-mesenchymal transition (EMT) contributes to the progression of renal tubulointerstitial fibrosis. The N-methyl-D-aspartate receptor (NMDAR), which is present in proximal tubular epithelium, is a glutamate receptor that acts as a calcium channel. Activation of NMDAR induces actin rearrangement in cells of the central nervous system, but whether it helps maintain the epithelial phenotype of the proximal tubule is unknown. Here, knockdown of NMDAR1 in a proximal tubule cell line (HK-2) induced changes in cell morphology, reduced E-cadherin expression, and increased ␣-SMA expression. Induction of EMT with TGF-␤1 led to downregulation of both E-cadherin and membrane-associated ␤-catenin, reorganization of F-actin, expression of mesenchymal markers de novo, upregulation of Snail1, and increased cell migration; co-treatment with NMDA attenuated all of these changes. Furthermore, NMDA reduced TGF-␤1-induced phosphorylation of Erk1/2 and Akt and the activation of Ras, suggesting that NMDA antagonizes TGF-␤1-induced EMT by inhibiting the Ras-MEK pathway. In the unilateral ureteral obstruction model, treatment with NMDA blunted obstruction-induced upregulation of ␣-SMA, FSP1, and collagen I and downregulation of E-cadherin. Taken together, these results suggest that NMDAR plays a critical role in preserving the normal epithelial phenotype and modulating tubular EMT.

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Relationship between GABAergic interneurons migration and early neocortical network activity

Lima

Gieseler

Voigt

2008

Developmental Neurobiology

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Available evidence converges to suggest that during the early development of the cerebral cortex, the emergence of the spontaneous network activity chronologically overlap with the end of the cell migration period in the developing cortex. We approached the functional regulation of neuronal migration in a culture model of neocortical networks, using time lapses to detect migratory movements, calcium-imaging to assess the activity of migratory neurons, and immunocytochemical methods to identify the migratory cells retrospectively. In cell cultures, early physiological development and cell migration are reproduced at a local network level, thus allowing the study of the interrelationships between cell migration and network development independent of the topographical complexity. Neurons migrate at least until 12 days in vitro and GABAergic neurons migrate faster compared with non-GABAergic neurons. A decline of migratory activity was coincident with the development of spontaneous synchronous network activity. Migrating interneurons did not participate in synchronous network activity, but interneurons that ended cell migration during observation time frequently engaged in synchronous activity within less than an hour. Application of GABA(A) and ionotropic glutamate receptor antagonists significantly increased the number of migrating GABAergic neurons without changing the dynamics of the migratory movements. Thus, neurotransmitters released by early network activity might favor the termination of neuronal migration. These results reinforce the idea that network activity plays an important role in the development of late-born GABAergic cells.

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Stimulation of N-methyl-d-aspartate (NMDA) receptors inhibits neuronal migration in embryonic cerebral cortex: a tissue culture study

Cited by 24 publications

References 9 publications

A Noncanonical Release of GABA and Glutamate Modulates Neuronal Migration

A Noncanonical Release of GABA and Glutamate Modulates Neuronal Migration

Glutamatergic Signaling Maintains the Epithelial Phenotype of Proximal Tubular Cells

Relationship between GABAergic interneurons migration and early neocortical network activity

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