Calcium‐permeable presynaptic AMPA receptors in cerebellar molecular layer interneurones

Rossi, Bénédicte; Maton, Gilliane; Collin, Thibault

doi:10.1113/jphysiol.2008.159921

Cited by 42 publications

(37 citation statements)

References 61 publications

(124 reference statements)

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“…Consequently, concerted stimulation of a bundle of PFs results in a homogeneous elevated glutamate concentration in the molecular layer that decreases relatively slowly because of the inefficiency of removal by diffusion (Barbour and Häusser, 1997). This elevated glutamate generated by repetitive stimulation of PFs has been shown to stimulate various ionotropic receptors in MLIs (Carter and Regehr, 2000;Rossi et al, 2008). Repetitive PF stimulation also can induce an inward current in these neurons, with a pharmacological profile consistent with the activation of mGluR1 (Karakossian and Otis, 2004).…”

Section: Resultsmentioning

confidence: 99%

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Activation of Metabotropic Glutamate Receptors Induces Periodic Burst Firing and Concomitant Cytosolic Ca²⁺Oscillations in Cerebellar Interneurons

Collin¹,

Franconville²,

Ehrlich³

et al. 2009

J. Neurosci.

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Section: Resultsmentioning

confidence: 99%

“…Results have been pooled together. In preliminary experiments, we verified using WCRs that this type of electrical stimulation elicited synaptic currents consistent with those described previously for PF-MLI synapses (Carter and Regehr, 2000;Rossi et al, 2008).…”

Section: Introductionmentioning

confidence: 90%

Activation of Metabotropic Glutamate Receptors Induces Periodic Burst Firing and Concomitant Cytosolic Ca²⁺Oscillations in Cerebellar Interneurons

Collin¹,

Franconville²,

Ehrlich³

et al. 2009

J. Neurosci.

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“…To determine the contribution of GluA2-lacking AMPARs to synaptic AMPAR activity of dorsal horn neurons, we used IEM-1460, a selective blocker of GluA2-lacking AMPARs (Samoilova et al, 1999;Rossi et al, 2008). Bath application of IEM-1460 (100 mM) for 6-8 minutes normalized the rectification index of AMPAR-EPSCs of lamina II neurons in SNL rats (0.89 6 0.06; Fig.…”

Section: Resultsmentioning

confidence: 99%

Nerve Injury Increases GluA2-Lacking AMPA Receptor Prevalence in Spinal Cords: Functional Significance and Signaling Mechanisms

Chen

Zhou

Byun

et al. 2013

The Journal of Pharmacology and Experimental Therapeutics

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The glutamate a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPARs) are critically involved in the excitatory synaptic transmission, and blocking AMPARs at the spinal level reverses neuropathic pain. However, little is known about changes in the composition of synaptic AMPARs in the spinal dorsal horn after peripheral nerve injury. AMPARs lacking the GluA2 subunit are permeable to Ca 21 , and their currents show unique inward rectification. We found that AMPARmediated excitatory postsynaptic currents (AMPAR-EPSCs) of spinal dorsal horn neurons exhibited a linear current-voltage relationship in control rats, whereas AMPAR-EPSCs of dorsal horn neurons displayed inward rectification in rats with spinal nerve injury. In nerve-injured rats, compared with control rats, the GluA2 protein level was significantly less in the plasma membrane but was greater in the cytosolic vesicle fraction in the dorsal spinal cord. However, the GluA1 protein levels in these fractions did not differ significantly between nerve-injured and control rats. Blocking N-methyl-D-aspartate receptors (NMDARs) abolished inward rectification of AMPAR-EPSCs of dorsal horn neurons in nerve-injured rats. Furthermore, inhibition of calpain or calcineurin, but not protein kinase C, completely blocked nerve injury-induced inward rectification of AMPAR-EPSCs of dorsal horn neurons. In addition, blocking GluA2-lacking AMPARs at the spinal cord level reduced nerve injury-induced pain hypersensitivity. Our study suggests that nerve injury increases GluA2 internalization and the prevalence of GluA2-lacking AMPARs in the spinal dorsal horn to maintain chronic neuropathic pain. Increased prevalence of spinal GluA2-lacking AMPARs in neuropathic pain is mediated by NMDARs and subsequent stimulation of calpain and calcineurin signaling.

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“…since both receptors are present at MLIs and are known to be Ca 2ϩ permeable in these neurons (Carter and Regehr 2000;Liu and Cull-Candy 2000;Rossi et al 2008;Shin and Linden 2005).…”

Section: Somatic [Ca 2ϩ ] I Signals From Mlis In Vivomentioning

confidence: 99%

Somatic calcium level reports integrated spiking activity of cerebellar interneurons in vitro and in vivo

Franconville

Revet

Astorga

et al. 2011

Journal of Neurophysiology

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We examined the relationship between somatic Ca 2ϩ signals and spiking activity of cerebellar molecular layer interneurons (MLIs) in adult mice. Using two-photon microscopy in conjunction with cell-attached recordings in slices, we show that in tonically firing MLIs loaded with high-affinity Ca 2ϩ probes, Ca 2ϩ -dependent fluorescence transients are absent. Spike-triggered averages of fluorescence traces for MLIs spiking at low rates revealed that the fluorescence change associated with an action potential is small (1% of the basal fluorescence ] i is not a direct readout of the firing activity, but rather reflects the time integral of this activity. MATERIALS AND METHODSAll experimental procedures were designed in accordance with the animal care guidelines of our host institution, which have been approved by the "Prefecture de Police" (approval number A-750607) following inspection by Veterinary Services of the City of Paris and by representatives of the French Ministry of Research and the Ministry for Health, in agreement with European Directive 86/609/EEC regarding the protection of animals used for experimental and other scientific purposes. In Vitro Patch-Clamp Recording and ImagingSlice preparation. Sagittal cerebellar slices (200 m thick) were prepared from C57BL/6J mice and from PVϪ/Ϫ mice. The PVϪ/Ϫ animals are congenic with C57BL/6J, after 10 matings of heterozygous (PVϩ/Ϫ) mice with wild-type C57BL/6J animals (Moreno et al 2011). Mice aged 22-33 days were decapitated after cervical dislocation. Slices were cut at 4°C in a saline solution of the following composition (in mM): 87 NaCl, 2.5 KCl, 1.25 NaH 2 PO 4 , 25 NaHCO 3 ,

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Calcium‐permeable presynaptic AMPA receptors in cerebellar molecular layer interneurones

Cited by 42 publications

References 61 publications

Activation of Metabotropic Glutamate Receptors Induces Periodic Burst Firing and Concomitant Cytosolic Ca²⁺Oscillations in Cerebellar Interneurons

Activation of Metabotropic Glutamate Receptors Induces Periodic Burst Firing and Concomitant Cytosolic Ca²⁺Oscillations in Cerebellar Interneurons

Nerve Injury Increases GluA2-Lacking AMPA Receptor Prevalence in Spinal Cords: Functional Significance and Signaling Mechanisms

Somatic calcium level reports integrated spiking activity of cerebellar interneurons in vitro and in vivo

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Calcium‐permeable presynaptic AMPA receptors in cerebellar molecular layer interneurones

Cited by 42 publications

References 61 publications

Activation of Metabotropic Glutamate Receptors Induces Periodic Burst Firing and Concomitant Cytosolic Ca2+Oscillations in Cerebellar Interneurons

Activation of Metabotropic Glutamate Receptors Induces Periodic Burst Firing and Concomitant Cytosolic Ca2+Oscillations in Cerebellar Interneurons

Nerve Injury Increases GluA2-Lacking AMPA Receptor Prevalence in Spinal Cords: Functional Significance and Signaling Mechanisms

Somatic calcium level reports integrated spiking activity of cerebellar interneurons in vitro and in vivo

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Activation of Metabotropic Glutamate Receptors Induces Periodic Burst Firing and Concomitant Cytosolic Ca²⁺Oscillations in Cerebellar Interneurons

Activation of Metabotropic Glutamate Receptors Induces Periodic Burst Firing and Concomitant Cytosolic Ca²⁺Oscillations in Cerebellar Interneurons