Ca signaling in astrocytes is considered to be mainly mediated by metabotropic receptors linked to intracellular Ca release. However, recent studies demonstrate a significant contribution of Ca influx to spontaneous and evoked Ca signaling in astrocytes, suggesting that Ca influx might account for astrocytic Ca signaling to a greater extent than previously thought. Here, we investigated AMPA-evoked Ca influx into olfactory bulb astrocytes in mouse brain slices using Fluo-4 and GCaMP6s, respectively. Bath application of AMPA evoked Ca transients in periglomerular astrocytes that persisted after neuronal transmitter release was inhibited by tetrodotoxin and bafilomycin A1. Withdrawal of external Ca suppressed AMPA-evoked Ca transients, whereas depletion of Ca stores had no effect. Both Ca transients and inward currents induced by AMPA receptor activation were partly reduced by Naspm, a blocker of Ca-permeable AMPA receptors lacking the GluA2 subunit. Antibody staining revealed a strong expression of GluA1 and GluA4 and a weak expression of GluA2 in periglomerular astrocytes. Our results indicate that Naspm-sensitive, Ca-permeable AMPA receptors contribute to Ca signaling in periglomerular astrocytes in the olfactory bulb.
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http://dx.doi.org/10.1038/srep44817 | DOI Listing |
J Neurosci
March 2019
College of Pharmacy, University of Texas at Austin, Austin, Texas 78712.
A growing number of studies implicate alterations in glutamatergic signaling within the reward circuitry of the brain during alcohol abuse and dependence. A key integrator of glutamatergic signaling in the reward circuit is the nucleus accumbens, more specifically, the dopamine D1 receptor-expressing medium spiny neurons (D1-MSNs) within this region, which have been implicated in the formation of dependence to many drugs of abuse including alcohol. D1-MSNs receive glutamatergic input from several brain regions; however, it is not currently known how individual inputs onto D1-MSNs are altered by alcohol experience.
View Article and Find Full Text PDFBiochim Biophys Acta Mol Basis Dis
July 2017
Institute of Biophysics, Biological Research Centre of the Hungarian Academy of Sciences, Temesvári krt. 62, 6726 Szeged, Hungary. Electronic address:
Increased intracellular calcium (Ca), which might be the consequence of an excess influx through Ca-permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, plays a crucial role in degeneration of motor neurons. Previously we demonstrated that the presymptomatic application of AMPA receptor antagonist, talampanel, could reduce Ca elevation in spinal motor neurons of mice carrying the G93A mutation of superoxide dismutase 1 (SOD1), modeling amyotrophic lateral sclerosis (ALS). It remained to be examined whether the remote, functionally semi-autonomous motor axon terminals could be rescued from the Ca overload, or if the terminals, where the degeneration possibly starts, already experience intractable changes at early time points.
View Article and Find Full Text PDFeNeuro
October 2017
Department of Cell Biology and Anatomy, LSU Health Sciences Center New Orleans, New Orleans, Louisiana 70112.
The fluorescent dyes, Alexa Fluor 488 and 594 are commonly used to visualize dendritic structures and the localization of synapses, both of which are critical for the spatial and temporal integration of synaptic inputs. However, the effect of the dyes on synaptic transmission is not known. Here we investigated whether Alexa Fluor dyes alter the properties of synaptic currents mediated by two subtypes of AMPA receptors (AMPARs) at cerebellar stellate cell synapses.
View Article and Find Full Text PDFJ Neurosurg
April 2013
Department of Neurosurgery, Faculty of Clinical Medicine, University of the Ryukyus, Okinawa, Japan.
Object: Blockade of Ca(++)-permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptor (AMPAR) inhibits the proliferation of human glioblastoma by inhibiting Akt phosphorylation, which is independent of the phosphatidylinositol 3-kinase pathway. Inhibiting platelet-derived growth factor receptor (PDGFR)-mediated phosphorylation causes growth inhibition in glioblastoma cells. The authors of this study investigated the effects of YM872 and AG1296, singly and in combination and targeting different pathways upstream of Akt, on Akt-mediated tumor growth in glioblastoma cells in vivo and in vitro.
View Article and Find Full Text PDFRoss Fiziol Zh Im I M Sechenova
July 2012
The effects of non-competitive glutamate receptor antagonists on sleep-waking organization have been studied on Krushinskii-Molodkina rats having an inherited predisposition to audiogenic seizures and Wistar ones which are resistant to this action of sound. Two types of blockers of glutamate receptor open channels were used: selective blockers of NMDA receptors (memantine and IEM-1921) and blockers of mixed type, impacting both on the NMDA and Ca-permeable AMPA/ kainate receptors (IEM-1754 and IEM 1925). During the first 3 hours after administration of these glutamate antagonists the total or partial deprivation of fast-wave sleep was provoked.
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