Action of extracellular divalent cations on native α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate (AMPA) receptors

Дорофеева, Н. А.; Tikhonov, Denis B.; Barygin, Oleg I.; Tikhonova, Tatiana B.; Sal'nikov, Yu. I.; Lg, Magazanik

doi:10.1111/j.1471-4159.2005.03533.x

Cited by 10 publications

(12 citation statements)

References 31 publications

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“…Recently it has been demonstrated that divalent cations can act like competitive antagonists at the AMPA receptor (Dorofeeva et al, 2005). The effect we report in this study is a reduction in AMPA current with lowering of [Ca 2ϩ ] ec .…”

Section: The Mechanism For the Change In Quantal Sizesupporting

confidence: 59%

Extracellular Calcium Regulates Postsynaptic Efficacy through Group 1 Metabotropic Glutamate Receptors

Hardingham

Bannister

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et al. 2006

Journal of Neuroscience

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Bursts of synaptic transmission are known to induce transient depletion of Ca2ϩ within the synaptic cleft. Although Ca 2ϩ depletion has been shown to lower presynaptic release probability, effects on the postsynaptic cell have not been reported. In this study, we show that physiologically relevant reductions in extracellular Ca 2ϩ lead to a decrease in synaptic strength between synaptically coupled layer 2/3 cortical pyramidal neurons. Using quantal analysis and mEPSP analysis, we demonstrate that a lowered extracellular Ca 2ϩ produces a reduction in the postsynaptic quantal size in addition to its known effect on release probability. An elevated Mg 2ϩ level can prevent this reduction in postsynaptic efficacy at subphysiological Ca 2ϩ levels. We show that the calcium-dependent effect on postsynaptic quantal size is mediated by group 1 metabotropic glutamate receptors, acting via CaMKII (Ca 2ϩ /calmodulin-dependent protein kinase II) and PKC. Therefore, physiologically relevant changes in extracellular Ca 2ϩ can regulate information transfer at cortical synapses via both presynaptic and postsynaptic mechanisms.

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Section: The Mechanism For the Change In Quantal Sizesupporting

confidence: 59%

Extracellular Calcium Regulates Postsynaptic Efficacy through Group 1 Metabotropic Glutamate Receptors

Hardingham

Bannister

Read

et al. 2006

Journal of Neuroscience

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“…The proposed mechanism of action is that complexes of divalent cations and AMPAR agonists compete with the free agonists rather than the cations themselves. This mechanism fits the data in which a competitive type of inhibition is observed; in addition, an increase in agonist concentration reduce the inhibitory effects of divalent metals less than that of DNQX (the classical competitive AMPAR antagonist) [190].…”

Section: Ampa and Kainate Receptorssupporting

confidence: 84%

“…Various metals caused inhibition of Ca 2+ impermeable AMPA-R, the inhibition was fast, reversible, and voltage independent. The rank order of activities was Ni 2+ > Zn 2+ > Co 2+ > Ca 2+ > Mn 2+ > Mg 2+ [190]. The proposed mechanism of action was that complexes of AMPAR agonists and divalent cations compete with the free agonists for the binding sites.…”

Section: Discussionmentioning

confidence: 99%

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Metal toxicity at the synapse: presynaptic, postsynaptic and long-term effects

Ghazala

Sadiq

Chowdhury

et al. 2010

Qatar Foundation Annual Research Forum Proceedings

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Metal neurotoxicity is a global health concern. This paper summarizes the evidence for metal interactions with synaptic transmission and synaptic plasticity. Presynaptically metal ions modulate neurotransmitter release through their interaction with synaptic vesicles, ion channels, and the metabolism of neurotransmitters (NT). Many metals (e.g., Pb 2+ , Cd 2+ , and Hg + ) also interact with intracellular signaling pathways. Postsynaptically, processes associated with the binding of NT to their receptors, activation of channels, and degradation of NT are altered by metals. Zn 2+ , Pb 2+ , Cu 2+ , Cd 2+ , Ni 2+ , Co 2+ , Li 3+ , Hg + , and methylmercury modulate NMDA, AMPA/kainate, and/or GABA receptors activity. Al 3+ , Pb 2+ , Cd 2+ , and As 2 O 3 also impair synaptic plasticity by targeting molecules such as CaM, PKC, and NOS as well as the transcription machinery involved in the maintenance of synaptic plasticity. The multiple effects of metals might occur simultaneously and are based on the specific metal species, metal concentrations, and the types of neurons involved.

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“…Injection of magnesium 15 min after picrotoxin virtually did not modify the hyperkinetic effects of picrotoxin. The results indicate the role of calcium processes in the appearance of strial picrotoxin hyperactivity and principal possibility of its correction with magnesium only before the cascade of respective calcium ionic transformations is triggered in the brain.Bivalent magnesium, zinc, and cobalt ions are the most effective blockers of calcium channels [6,9]. Our previous studies [1,4,5] showed that one of the mechanisms of hyperkinesia caused in rats by microinjection of picrotoxin (PT; GABA A receptor antagonist) into the neostriatum (NS) is distortion of neuronal calcium homeostasis.…”

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confidence: 99%

Intrastrial injection of magnesium after picrotoxin does not reduce motor hyperactivity in rats

2008

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Magnesium chloride injected into rat rostral neostriatum before picrotoxin prevents motor hyperactivity induced by this GABAA receptor antagonist: prevents the increase in spontaneous motor activity in the open field test and reduces reproduction and duration of choreic hyperkinesia. Injection of magnesium 15 min after picrotoxin virtually did not modify the hyperkinetic effects of picrotoxin. The results indicate the role of calcium processes in the appearance of strial picrotoxin hyperactivity and principal possibility of its correction with magnesium only before the cascade of respective calcium ionic transformations is triggered in the brain.

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Action of extracellular divalent cations on native α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate (AMPA) receptors

Abstract: The effects of divalent cations on Ca 2+ -impermeable containing (GluR2 subunit) MPA receptors of hippocampal pyramidal neurones isolated from rat brain was studied using patch-clamping.

Cited by 10 publications

References 31 publications

Extracellular Calcium Regulates Postsynaptic Efficacy through Group 1 Metabotropic Glutamate Receptors

Extracellular Calcium Regulates Postsynaptic Efficacy through Group 1 Metabotropic Glutamate Receptors

Metal toxicity at the synapse: presynaptic, postsynaptic and long-term effects

Intrastrial injection of magnesium after picrotoxin does not reduce motor hyperactivity in rats

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