Influence of external magnesium ions on the NMDA receptor channel block by different types of organic cations

Nikolaev, Maxim V.; Lg, Magazanik; Tikhonov, Denis B.

doi:10.1016/j.neuropharm.2011.12.029

Cited by 55 publications

(25 citation statements)

References 33 publications

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“…7,[9][10][11] Evidences from previous studies suggested that NMDA receptors are involved in the plasticity that arises from the long-term administration of morphine. [20][21][22][23][24] In the present study pretreatment with Magnesium sulfate (20,40 and 60 mg/kg, ip) 30 min before daily Morphine administration reduced tolerance and dependency of Morphine. Chronic Morphine administration induces down regulation of spinal GTs and as a result Morphine-induced GT down regulation would increase the availability of extracellular glutamate.…”

Section: Discussionsupporting

confidence: 45%

“…Increased glutamate availability at the extracellular level could increase the probability of excitatory amino acid receptor activation including NMDARs. 20,[23][24][25][26] Amitriptyline might attenuate the development of morphine dependency and tolerance. The proposed mechanisms are including: Inhibiting of the expression of pro-inflammatory cytokines such as TNFα, IL-1β, and IL-6 and increasing expression of IL-10 via the p38 MAPK-HO-1 signal transduction cascade; Activation of NF-κB, inhibiting glutamate transporter downregulation, and expression of up-regulating of glutamate transporters GLAST and GLT-1 in glial cells; and finally preventing phospho-PKA and PKC expression, thus promoting GLAST and GLT-1 trafficking to the glial cell surface.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Attenuation of Morphine-Induced Tolerance and Dependency by Pretreatment with Magnesium Sulfate and Amitriptyline in Male Mice

Habibiasl¹,

Vaez²,

Aghaie³

et al. 2015

Pharm Sci

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Section: Discussionsupporting

confidence: 45%

Section: Discussionmentioning

confidence: 99%

Attenuation of Morphine-Induced Tolerance and Dependency by Pretreatment with Magnesium Sulfate and Amitriptyline in Male Mice

Habibiasl¹,

Vaez²,

Aghaie³

et al. 2015

Pharm Sci

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“…Because both memantine's and ketamine's binding site in the NMDAR channel (Figure 1) overlaps with the Mg 2+ binding site, Mg 2+ competes with both drugs for binding to NMDAR channels. As a result, physiological concentrations of Mg 2+ (∼1 mM) substantially increase the IC 50 , modify the voltage dependence, and alter the NMDAR subtype-selectivity of both memantine and ketamine [16-18]. …”

Section: Nmdars and Their Inhibition By Memantine And Ketaminementioning

confidence: 99%

Recent insights into the mode of action of memantine and ketamine

Johnson

Glasgow

Povysheva

2015

Current Opinion in Pharmacology

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The clinical benefits of the glutamate receptor antagonists memantine and ketamine have helped sustain optimism that glutamate receptors represent viable targets for development of therapeutic drugs. Both memantine and ketamine antagonize N-methyl-d-aspartate receptors (NMDARs), a glutamate receptor subfamily, by blocking the receptor-associated ion channel. Although many of the basic characteristics of NMDAR inhibition by memantine and ketamine appear similar, their effects on humans and to a lesser extent on rodents are strongly divergent. Some recent research suggests that preferential inhibition by memantine and ketamine of distinct NMDAR subpopulations may contribute to the drugs' differential clinical effects. Here we review studies that shed light on possible explanations for differences between the effects of memantine and ketamine.

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“…The molecular mechanism of the interaction of these blockers with glutamate-activated NMDA receptors has been studied in detail [17][18][19]. Adamantane derivatives (memantine and IEM-1958) and a phenylcyclohexyl derivative (IEM-1921) produce voltage-dependent blockade of the open state of the NMDA receptor channel [12,[17][18][19][20], competing with magnesium ions [36,46]. These blockers are characterized by high selectivity in relation to open NMDA-type glutamate receptor channels [18].…”

Section: Discussionmentioning

confidence: 99%

The Ability of NMDA-Type Glutamate Receptor Blockers to Prevent the Development of Pentylenetetrazole Kindling and Morphological Changes to Pyramidal Neurons in the Mouse Hippocampus

Vasilev

Туманова

Lavrent’eva

et al. 2015

Neurosci Behav Physi

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Experiments on mice addressed the link between convulsive syndrome and morphological changes in hippocampal neurons occurring on development of pentylenetetrazole (PTZ) kindling. Kindling was induced by i.p. PTZ (35 mg/kg) three times a week for one month. By the end of this period, 70% of the mice responded to administration of PTZ with severe clonic or clonic-tonic seizures. Hippocampal sections (stratum pyramidale, field CA1, Nissl staining) from convulsive mice showed large numbers of altered cells (24.7 ± 2.1%). Most of these were pyramidal neurons. These hyperchromic neurons had reduced body sizes, loss of turgor, wrinkling of the cell body, and deformation of dendritic processes. These dark-type changes were present in 2.3 ± 2.1% of neurons in the hippocampus of intact mice and mice resistant to the convulsogenic effect of PTZ (30% of the population). Immunohistochemical studies demonstrated normal expression of NeuN (Fox3) protein in all hippocampal cells, including dark hyperchromic neurons. This is evidence that neurons did not die en masse and were relatively viable. Prophylactic s.c. administration of NMDA receptor blockers (0.5 mg/kg memantine, 0.1 mg/kg IEM-1921, or 1 mg/kg IEM-1958) decreased the proportion of mice developing PTZ kindling from 70% to 40%. The proportion of altered neurons in the 60% of mice given NMDA blockers and not developing PTZ kindling or convulsions in the presence of blockers was 0.1 ± 0.06%, which was the same as in intact mice. Conversely, the hippocampus of mice demonstrating convulsions despite simultaneous administration of NMDA blockers showed 24.0 ± 5.6% hyperchromic neurons. These results provide evidence that pathologically altered neurons appeared after convulsive seizures in animals after PTZ kindling and that blockade of NMDA glutamate receptors could weaken both the development of convulsive syndrome and the concomitant morphological changes to hippocampal neurons.

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Influence of external magnesium ions on the NMDA receptor channel block by different types of organic cations

Cited by 55 publications

References 33 publications

Attenuation of Morphine-Induced Tolerance and Dependency by Pretreatment with Magnesium Sulfate and Amitriptyline in Male Mice

Attenuation of Morphine-Induced Tolerance and Dependency by Pretreatment with Magnesium Sulfate and Amitriptyline in Male Mice

Recent insights into the mode of action of memantine and ketamine

The Ability of NMDA-Type Glutamate Receptor Blockers to Prevent the Development of Pentylenetetrazole Kindling and Morphological Changes to Pyramidal Neurons in the Mouse Hippocampus

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