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  • 1
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    Pharmacological characterization, localization, and regulation of ionotropic glutamate receptors in skate horizontal cells
    Cambridge University Press (CUP) ; 2009
    In:  Visual Neuroscience Vol. 26, No. 4 ( 2009-07), p. 375-387
    Details
    In: Visual Neuroscience, Cambridge University Press (CUP), Vol. 26, No. 4 ( 2009-07), p. 375-387
    Abstract: Glutamate is believed to be the primary excitatory neurotransmitter in the vertebrate retina, and its fast postsynaptic effects are elicited by activating NMDA-, kainate-, or AMPA-type glutamate receptors. We have characterized the ionotropic glutamate receptors present on retinal horizontal cells of the skate, which possess a unique all-rod retina simplifying synaptic circuitry within the outer plexiform layer (OPL). Isolated external horizontal cells were examined using whole-cell voltage-clamp techniques. Glutamate and its analogues kainate and AMPA, but not NMDA, elicited dose-dependent currents. The AMPA receptor antagonist GYKI 52466 at 100 μ m abolished glutamate-elicited currents. Desensitization of glutamate currents was removed upon coapplication of cyclothiazide, known to potentiate AMPA receptor responses, but not by concanavalin A, which potentiates kainate receptor responses. The dose–response curve to glutamate was significantly broader in the presence of the desensitization inhibitor cyclothiazide. Polyclonal antibodies directed against AMPA receptor subunits revealed prominent labeling of isolated external horizontal cells with the GluR2/3 and GluR4 antibodies. 1-Naphthylacetyl spermine, known to block calcium-permeable AMPA receptors, significantly reduced glutamate-gated currents of horizontal cells. Downregulation of glutamate responses was induced by increasing extracellular ion concentrations of Zn 2+ and H + . The present study suggests that Ca 2+ -permeable AMPA receptors likely play an important role in shaping the synaptic responses of skate horizontal cells and that alterations in extracellular concentrations of calcium, zinc, and hydrogen ions have the potential to regulate the strength of postsynaptic signals mediated by AMPA receptors within the OPL.
    Type of Medium: Online Resource
    ISSN: 0952-5238 , 1469-8714
    URL: Article
    DOI: 10.1017/S0952523809990149
    RVK:
    WA 15000
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2009
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    SSG: 12
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  • 2
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    Review and Hypothesis: A Potential Common Link Between Glial Cells, Calcium Changes, Modulation of Synaptic Transmission, Spreading Depression, Migraine, and Epilepsy—H+
    Frontiers Media SA ; 2021
    In:  Frontiers in Cellular Neuroscience Vol. 15 ( 2021-9-3)
    Details
    In: Frontiers in Cellular Neuroscience, Frontiers Media SA, Vol. 15 ( 2021-9-3)
    Abstract: There is significant evidence to support the notion that glial cells can modulate the strength of synaptic connections between nerve cells, and it has further been suggested that alterations in intracellular calcium are likely to play a key role in this process. However, the molecular mechanism(s) by which glial cells modulate neuronal signaling remains contentiously debated. Recent experiments have suggested that alterations in extracellular H + efflux initiated by extracellular ATP may play a key role in the modulation of synaptic strength by radial glial cells in the retina and astrocytes throughout the brain. ATP-elicited alterations in H + flux from radial glial cells were first detected from Müller cells enzymatically dissociated from the retina of tiger salamander using self-referencing H + -selective microelectrodes. The ATP-elicited alteration in H + efflux was further found to be highly evolutionarily conserved, extending to Müller cells isolated from species as diverse as lamprey, skate, rat, mouse, monkey and human. More recently, self-referencing H + -selective electrodes have been used to detect ATP-elicited alterations in H + efflux around individual mammalian astrocytes from the cortex and hippocampus. Tied to increases in intracellular calcium, these ATP-induced extracellular acidifications are well-positioned to be key mediators of synaptic modulation. In this article, we examine the evidence supporting H + as a key modulator of neurotransmission, review data showing that extracellular ATP elicits an increase in H + efflux from glial cells, and describe the potential signal transduction pathways involved in glial cell—mediated H + efflux. We then examine the potential role that extracellular H + released by glia might play in regulating synaptic transmission within the vertebrate retina, and then expand the focus to discuss potential roles in spreading depression, migraine, epilepsy, and alterations in brain rhythms, and suggest that alterations in extracellular H + may be a unifying feature linking these disparate phenomena.
    Type of Medium: Online Resource
    ISSN: 1662-5102
    URL: Article
    DOI: 10.3389/fncel.2021.693095
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2452963-1
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  • 3
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    Glutamate modulation of GABA transport in retinal horizontal cells of the skate
    Wiley ; 2003
    In:  The Journal of Physiology Vol. 546, No. 3 ( 2003-02), p. 717-731
    Details
    In: The Journal of Physiology, Wiley, Vol. 546, No. 3 ( 2003-02), p. 717-731
    Abstract: Transport of the amino acid GABA into neurons and glia plays a key role in regulating the effects of GABA in the vertebrate retina. We have examined the modulation of GABA‐elicited transport currents of retinal horizontal cells by glutamate, the likely neurotransmitter of vertebrate photoreceptors. Enzymatically isolated external horizontal cells of skate were examined using whole‐cell voltage‐clamp techniques. GABA (1 m m ) elicited an inward current that was completely suppressed by the GABA transport inhibitors tiagabine (10 μ m ) and SKF89976‐A (100 μ m ), but was unaffected by 100 μ m picrotoxin. Prior application of 100 μ m glutamate significantly reduced the GABA‐elicited current. Glutamate depressed the GABA dose‐response curve without shifting the curve laterally or altering the voltage dependence of the current. The ionotropic glutamate receptor agonists kainate and AMPA also reduced the GABA‐elicited current, and the effects of glutamate and kainate were abolished by the ionotropic glutamate receptor antagonist 6‐cyano‐7‐nitroquinoxaline. NMDA neither elicited a current nor modified the GABA‐induced current, and metabotropic glutamate analogues were also without effect. Inhibition of the GABA‐elicited current by glutamate and kainate was reduced when extracellular calcium was removed and when recording pipettes contained high concentrations of the calcium chelator BAPTA. Caffeine (5 m m ) and thapsigargin (2 n m ), agents known to alter intracellular calcium levels, also reduced the GABA‐elicited current, but increases in calcium induced by depolarization alone did not. Our data suggest that glutamate regulates GABA transport in retinal horizontal cells through a calcium‐dependent process, and imply a close physical relationship between calcium‐permeable glutamate receptors and GABA transporters in these cells.
    Type of Medium: Online Resource
    ISSN: 0022-3751 , 1469-7793
    URL: Article
    DOI: 10.1113/jphysiol.2002.034421
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2003
    detail.hit.zdb_id: 1475290-6
    SSG: 12
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  • 4
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    Activation of retinal glial (Müller) cells by extracellular ATP induces pronounced increases in extracellular H+ flux
    Public Library of Science (PLoS) ; 2018
    In:  PLOS ONE Vol. 13, No. 2 ( 2018-2-21), p. e0190893-
    Details
    In: PLOS ONE, Public Library of Science (PLoS), Vol. 13, No. 2 ( 2018-2-21), p. e0190893-
    Type of Medium: Online Resource
    ISSN: 1932-6203
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.1371/journal.pone.0190893
    DOI: 10.1371/journal.pone.0190893.g001
    DOI: 10.1371/journal.pone.0190893.g002
    DOI: 10.1371/journal.pone.0190893.g003
    DOI: 10.1371/journal.pone.0190893.g004
    DOI: 10.1371/journal.pone.0190893.g005
    DOI: 10.1371/journal.pone.0190893.g006
    Language: English
    Publisher: Public Library of Science (PLoS)
    Publication Date: 2018
    detail.hit.zdb_id: 2267670-3
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  • 5
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    Separation and light adaptation of rod and cone signals in the retina of the goldfish
    Elsevier BV ; 1986
    In:  Vision Research Vol. 26, No. 10 ( 1986-1), p. 1655-1666
    Details
    In: Vision Research, Elsevier BV, Vol. 26, No. 10 ( 1986-1), p. 1655-1666
    Type of Medium: Online Resource
    ISSN: 0042-6989
    URL: Article
    DOI: 10.1016/0042-6989(86)90053-2
    RVK:
    WW 1780
    RVK:
    WA 15000
    RVK:
    CP 2500
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1986
    detail.hit.zdb_id: 2011974-4
    SSG: 12
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  • 6
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    Proteins and lipids define the diffusional field of nitric oxide
    American Physiological Society ; 2001
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 281, No. 4 ( 2001-10-01), p. L904-L912
    Details
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 281, No. 4 ( 2001-10-01), p. L904-L912
    Abstract: Nitric oxide (NO) fluxes released from the surface of individual activated macrophages or cells localized in small aggregates were measured with a novel polarographic self-referencing microsensor. NO fluxes could be detected at distances from the cells of 100–500 μm. The initial flux and the distance from the cells at which NO could be detected were directly related to the number of cells in the immediate vicinity of the probe releasing NO. Thus, whereas NO fluxes of ∼1 pmol · cm −2 · s −1 were measured from individual macrophages, aggregates composed of groups of cells varying in number from 18 to 48 cells produced NO fluxes of between ∼4 and 10 pmol · cm −2 · s −1 . NO fluxes required the presence of l-arginine. Signals were significantly reduced by the addition of hemoglobin and by N-nitro-l-arginine methyl ester. NO fluxes were greatest when the sensor was placed immediately adjacent to cell membranes and declined as the distance from the cell increased. The NO signal was markedly reduced in the presence of the protein albumin but not by either oxidized or reduced glutathione. A reduction in the NO signal was also noted after the addition of lipid micelles to the culture medium. These results demonstrate that NO can be detected at significant distances from the cell of origin. In addition, both proteins and lipids strongly influence the net movement of free NO from macrophages. This suggests that these tissue components play an important role in regulating the biological activity of NO.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    URL: Article
    DOI: 10.1152/ajplung.2001.281.4.L904
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2001
    detail.hit.zdb_id: 1477300-4
    SSG: 12
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  • 7
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    Extracellular ATP-Induced Alterations in Extracellular H+ Fluxes From Cultured Cortical and Hippocampal Astrocytes
    Frontiers Media SA ; 2021
    In:  Frontiers in Cellular Neuroscience Vol. 15 ( 2021-4-30)
    Details
    In: Frontiers in Cellular Neuroscience, Frontiers Media SA, Vol. 15 ( 2021-4-30)
    Abstract: Small alterations in the level of extracellular H + can profoundly alter neuronal activity throughout the nervous system. In this study, self-referencing H + -selective microelectrodes were used to examine extracellular H + fluxes from individual astrocytes. Activation of astrocytes cultured from mouse hippocampus and rat cortex with extracellular ATP produced a pronounced increase in extracellular H + flux. The ATP-elicited increase in H + flux appeared to be independent of bicarbonate transport, as ATP increased H + flux regardless of whether the primary extracellular pH buffer was 26 mM bicarbonate or 1 mM HEPES, and persisted when atmospheric levels of CO 2 were replaced by oxygen. Adenosine failed to elicit any change in extracellular H + fluxes, and ATP-mediated increases in H + flux were inhibited by the P2 inhibitors suramin and PPADS suggesting direct activation of ATP receptors. Extracellular ATP also induced an intracellular rise in calcium in cultured astrocytes, and ATP-induced rises in both calcium and H + efflux were significantly attenuated when calcium re-loading into the endoplasmic reticulum was inhibited by thapsigargin. Replacement of extracellular sodium with choline did not significantly reduce the size of the ATP-induced increases in H + flux, and the increases in H + flux were not significantly affected by addition of EIPA, suggesting little involvement of Na + /H + exchangers in ATP-elicited increases in H + flux. Given the high sensitivity of voltage-sensitive calcium channels on neurons to small changes in levels of free H + , we hypothesize that the ATP-mediated extrusion of H + from astrocytes may play a key role in regulating signaling at synapses within the nervous system.
    Type of Medium: Online Resource
    ISSN: 1662-5102
    URL: Article
    DOI: 10.3389/fncel.2021.640217
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
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  • 8
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    ATP-mediated increase in H + flux from retinal Müller cells: a role for Na + /H + exchange
    American Physiological Society ; 2021
    In:  Journal of Neurophysiology Vol. 125, No. 1 ( 2021-01-01), p. 184-198
    Details
    In: Journal of Neurophysiology, American Physiological Society, Vol. 125, No. 1 ( 2021-01-01), p. 184-198
    Abstract: Small alterations in extracellular H + can profoundly alter neurotransmitter release by neurons. We examined mechanisms by which extracellular ATP induces an extracellular H + flux from Müller glial cells, which surround synaptic connections throughout the vertebrate retina. Müller glia were isolated from tiger salamander retinae and H + fluxes examined using self-referencing H + -selective microelectrodes. Experiments were performed in 1 mM HEPES with no bicarbonate present. Replacement of extracellular sodium by choline decreased H + efflux induced by 10 µM ATP by 75%. ATP-induced H + efflux was also reduced by Na + /H + exchange inhibitors. Amiloride reduced H + efflux initiated by 10 µM ATP by 60%, while 10 µM cariporide decreased H + flux by 37%, and 25 µM zoniporide reduced H + flux by 32%. ATP-induced H + fluxes were not significantly altered by the K + /H + pump blockers SCH28080 or TAK438, and replacement of all extracellular chloride with gluconate was without effect on H + fluxes. Recordings of ATP-induced H + efflux from cells that were simultaneously whole cell voltage clamped revealed no effect of membrane potential from −70 mV to 0 mV. Restoration of extracellular potassium after cells were bathed in 0 mM potassium produced a transient alteration in ATP-dependent H + efflux. The transient response to extracellular potassium occurred only when extracellular sodium was present and was abolished by 1 mM ouabain, suggesting that alterations in sodium gradients were mediated by Na + /K + -ATPase activity. Our data indicate that the majority of H + efflux elicited by extracellular ATP from isolated Müller cells is mediated by Na + /H + exchange. NEW & NOTEWORTHY Glial cells are known to regulate neuronal activity, but the exact mechanism(s) whereby these “support” cells modulate synaptic transmission remains unclear. Small changes in extracellular levels of acidity are known to be particularly powerful regulators of neurotransmitter release. Here, we show that extracellular ATP, known to be a potent activator of glial cells, induces H + efflux from retinal Müller (glial) cells and that the bulk of the H + efflux is mediated by Na + /H + exchange.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    URL: Article
    DOI: 10.1152/jn.00546.2020
    RVK:
    XA 10000 ; XA 552555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2021
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
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  • 9
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    Fluorescent imaging reports an extracellular alkalinization induced by glutamatergic activation of isolated retinal horizontal cells
    American Physiological Society ; 2014
    In:  Journal of Neurophysiology Vol. 111, No. 5 ( 2014-03-01), p. 1056-1064
    Details
    In: Journal of Neurophysiology, American Physiological Society, Vol. 111, No. 5 ( 2014-03-01), p. 1056-1064
    Abstract: Extracellular acidification induced by retinal horizontal cells has been hypothesized to underlie lateral feedback inhibition onto vertebrate photoreceptors. To test this hypothesis, the H + -sensitive fluorophore 5-hexadecanoylaminofluorescein (HAF) was used to measure changes in H + from horizontal cells isolated from the retina of the catfish. HAF staining conditions were modified to minimize intracellular accumulation of HAF and maximize membrane-associated staining, and ratiometric fluorescent imaging of cells displaying primarily membrane-associated HAF fluorescence was conducted. Challenge of such HAF-labeled cells with glutamate or the ionotropic glutamate receptor agonist kainate produced an increase in the fluorescence ratio, consistent with an alkalinization response of +0.12 pH units and +0.23 pH units, respectively. This alkalinization was blocked by the AMPA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), the L-type calcium channel blocker nifedipine, and lanthanum. The alkalinization reported by HAF was consistent with extracellular alkalinizations detected in previous studies using self-referencing H + -selective microelectrodes. The spatial distribution of the kainate-induced changes in extracellular H + was also examined. An overall global alkalinization around the cell was observed, with no obvious signs of discrete centers of acidification. Taken together, these data argue against the hypothesis that glutamatergic-induced efflux of protons from horizontal cells mediates lateral feedback inhibition in the outer retina.
    Type of Medium: Online Resource
    ISSN: 0022-3077 , 1522-1598
    URL: Article
    DOI: 10.1152/jn.00768.2013
    RVK:
    XA 10000 ; XA 552555
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2014
    detail.hit.zdb_id: 80161-6
    detail.hit.zdb_id: 1467889-5
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  • 10
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    Gap-junctional properties of electrically coupled skate horizontal cells in culture
    Cambridge University Press (CUP) ; 1993
    In:  Visual Neuroscience Vol. 10, No. 2 ( 1993-03), p. 287-295
    Details
    In: Visual Neuroscience, Cambridge University Press (CUP), Vol. 10, No. 2 ( 1993-03), p. 287-295
    Abstract: Whole-cell voltage-clamp recordings were used to examine the unusual pharmacological properties of the electrical coupling between rod-driven horizontal cells in skate retina as revealed previously by receptive-field measurements (Qian & Ripps, 1992). The junctional resistance was measured in electrically coupled cell pairs that had been enzymatically isolated and maintained in culture; the typical value was about 19.92 MΩ( n = 45), more than an order of magnitude lower than the nonjunctional membrane resistance. These data and the intercellular spread of the fluorescent dye Lucifer Yellow provide a good indication that skate horizontal cells are well coupled. The junctional conductance between cells was not modulated by the neurotransmitters dopamine (200 μM) or GABA (1 mM), nor was it affected by the membrane-permeable analogues of cAMP or cGMP, or the adenylate cyclase activator, forskolin. Although resistant to agents that have been reported to alter horizontal-cell coupling in cone-driven horizontal cells, the junctional conductance between paired horizontal cells of skate was greatly reduced by the application of 20 mM acetate, which is known to effectively reduce intracellular pH. Together with the results obtained in situ on the receptive-field properties of skate horizontal cells, these findings indicate that the gap-junctional properties of rod-driven horizontal cells of the skate are fundamentally different from those of cone-driven horizontal cells in other species. This raises the possibility that there is more than one class of electrical synapse on vertebrate horizontal cells.
    Type of Medium: Online Resource
    ISSN: 0952-5238 , 1469-8714
    URL: Article
    DOI: 10.1017/S0952523800003680
    RVK:
    WA 15000
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 1993
    detail.hit.zdb_id: 1489922-X
    SSG: 12
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