Functional interaction between various glutamate receptors

Boldyrev, Alexander A.

doi:10.1007/bf02682242

Cited by 4 publications

(5 citation statements)

References 28 publications

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“…728: 121-124, 1996). release, which is dependent on α(2+3) subunits of the Na + /K + -pump is only partially dependent on the protein kinase C family (PkC) and this partial dependence may be related to the stimulating PkC effect on NMDA receptors (Boldyrev, 2000). When the α1 subunit of Na + /K + -ATPase is additionally inhibited by ouabain, the larger portion of calcium ions is released, and partially insensitive to chelerithrine.…”

Section: Fig 3 Demonstrates How Different Inhibitors Affect the Ouabmentioning

confidence: 99%

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Glutamate receptors modulate oxidative stress in neuronal cells. A mini-review

2004

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Multiple lines of evidence demonstrate that reactive oxygen species (ROS) are involved in regulation of normal cell metabolism as second messengers. Under extreme conditions, these molecules induce oxidative stress, which may stimulate (or accompany) a number of neurodegenerative processes. In the glutamatergic system, ROS levels are under control of ionotropic and metabotropic glutamate receptors, which modulate ion fluxes through the neuronal membrane. The Na+/K(+)-pump is also one of the important participants affecting stationary ROS levels through several distinct mechanisms. This review describes the involvement of the Na+/K(+)-pump in intracellular signaling mechanisms via cross-talk between the pump and glutamate receptors in cerebellum granule cells. Selective dysfunction of mGlu II receptors may also lead to abnormal protein phosphorylation (i.e., tau phosphorylation), culminating in neurodegenerative disorders (i.e., Alzheimer disease). Also, unregulated production of intracellular ROS resulting from an imbalance of ionotropic and metabotropic receptors may activate one or more protein kinases. In summary, Glu receptor dysfunction, leading to a deficit in glutamate-mediated signal transduction may represent one of the earliest stages of neurodegenerative disorders. The Na+/K(+)-pump is able to prevent over-production of intracellular ROS, thus increasing oxidative stability of neuronal cells.

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Section: Fig 3 Demonstrates How Different Inhibitors Affect the Ouabmentioning

confidence: 99%

“…Such studies have demonstrated functional diversity of glutamate receptors but their interrelationships in cellular metabolism remain obscure (Boldyrev, 2000;Conn, 2003).…”

mentioning

confidence: 99%

Glutamate receptors modulate oxidative stress in neuronal cells. A mini-review

2004

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“…As shown in Figure 1 B, activation of calcium influx by the calcium ionophore ionomycin significantly increased the generation of the 110 kDa fragment, the NTF of N-cadherin in a dose-dependent manner. In general, NMDA is thought to activate ionotropic glutamate receptors that induce excess Ca 2ϩ influx in neurons (Boldyrev, 2000). To determine whether N-cadherin cleavage is associated with NMDA-mediated Ca 2ϩ influx, cortical neurons were incubated with NMDA.…”

Section: Nmda Receptor-induced Calcium Influx Increases N-cadherin CLmentioning

confidence: 99%

Calpain-Mediated N-Cadherin Proteolytic Processing in Brain Injury

Jang

Lee²,

Moon³

et al. 2009

J. Neurosci.

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Neural-cadherin (N-cadherin), a member of the classical cadherin family of transmembrane glycoproteins, mediates cellular recognition and cell-cell adhesion through calcium-dependent homophilic interactions and plays important roles in the development and maintenance of the nervous system. Metalloproteinase is known to cleave N-cadherin, which is further cleaved by ␥-secretase. The intracellular domain of N-cadherin interacts with ␤-catenin, and ␤-catenin stability is critical for cell-cell adhesion and cell survival. In the present study, we showed that N-cadherin is cleaved specifically by calpain, resulting in the generation of a novel 110 kDa fragment. The cleavage occurred in ischemic brain lesions and in vitro neural cells in the presence of NMDA and ionomycin, and was restored by calpain inhibitors but not matrix metalloproteinase or ␥-secretase inhibitors. Calpain directly cleaved N-cadherin in in vitro calpain assays, and calpain inhibitors prevented its cleavage in a dose-dependent manner. Using N-cadherin deletion mutants, we found that calpain cleavage sites exist in at least four regions of the cytoplasmic domain. Treatment with NMDA induced neuronal death, and it suppressed the expression of surface N-cadherin and the N-cadherin/␤-catenin interaction, effects that were prevented by calpain inhibitor. Furthermore, calpain-mediated N-cadherin cleavage significantly affected cell-cell adhesion, AKT signaling, the N-cadherin/␤-catenin interaction and the Wnt target gene expressions through the accumulation of nuclear ␤-catenin.

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“…The activation of PI-specific phospholipase C may be induced by the stimulation of metabotropic glutamate receptors and such activation depends on the availability of extracellular Ca 2+ [15]. In this aspect it is interesting to consider the hypothesis about the protective role of metabotropic glutamate receptors, considering that the activation of protein kinase C caused by stimulation of these receptors, leads to the phosphorylation (desensitization) of ionotropic NMDA-receptor [16], which play a leading role in the induction of ischemic damages due to their high affinity for excitatory amino acids (EAAs) and high permeability for Ca 2+ [17]. The stimulation of phospholipase C, initiated by neurotransmitters, is regulated by GTP-activated by G-protein, which links the receptor stimulus with the signaling pathway inside the cell.…”

Section: +mentioning

confidence: 99%

Dysregulation of Phospholipid Metabolism in Synaptic Membranes and Their Role in Encephalopathy Forming After a Hemorrhagic Shock

Leskova¹

2015

AJBIO

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Phospholipids (PLs) of neuronal membranes are active universal neuromodulators. They regulate many functions of the neurons, including receptors signaling, which during a hemorrhagic shock (HS) get damaged, leading to encephalopathy. An analysis of the data, presented in this review, suggests that the dysregulation of PL metabolism in synaptic membranes is a key mechanism of encephalopathy during HS. Stabilizing the PL composition of the neuronal membranes may become one of the most important treatment methods for shock-induced disorders of brain functions.

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Functional interaction between various glutamate receptors

Cited by 4 publications

References 28 publications

Glutamate receptors modulate oxidative stress in neuronal cells. A mini-review

Glutamate receptors modulate oxidative stress in neuronal cells. A mini-review

Calpain-Mediated N-Cadherin Proteolytic Processing in Brain Injury

Dysregulation of Phospholipid Metabolism in Synaptic Membranes and Their Role in Encephalopathy Forming After a Hemorrhagic Shock

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