Two types of glutamate receptors differentially excite amacrine cells in the tiger salamander retina.

Dixon, Donald B.; Copenhagen, David R.

doi:10.1113/jphysiol.1992.sp019103

Cited by 97 publications

(71 citation statements)

References 40 publications

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“…This may be especially true for different subtypes of retinal ACs (Dixon and Copenhagen, 1992). Here, we report the 4 levels, in the presence of CNQX (25 M) but in the absence of external Mg 2ϩ .…”

Section: Discussionmentioning

confidence: 90%

“…AMPARs and NMDARs are thought to be colocalized on the same AC bouton, although the relevant double-labeling immunohistochemical data published so far is not very extensive (Fletcher et al, 2000;Grunert et al, 2002). Moreover, electrophysiological studies have recorded NMDARmediated responses only in ACs that possessed AMPARs as well (Dixon and Copenhagen, 1992;Hartveit and Veruki, 1997;Matsui et al, 2001).…”

Section: Complementary Properties Of Glutamate and Gaba Receptorsmentioning

confidence: 99%

“…Amacrine cells possess AMPARs and NMDARs, and both contribute to their light response (Dixon and Copenhagen, 1992). A mixture of NBQX and AP-5 (25 and 50 M, respectively) completely eliminates the reciprocal feedback at the goldfish Mb terminal (Hull and von Gersdorff, 2004;Vigh et al, 2005).…”

Section: Desensitizing Ampars Trigger a Fast Gaba A Feedbackmentioning

confidence: 99%

“…In the CNS, the majority of fast excitatory transmission is mediated by non-NMDA glutamate receptors, whereas the NMDARs play a critical role in long-term synaptic plasticity (Collingridge and Lester, 1989). In the retina, AMPA and NMDARs are involved in mediating light responses in ACs (Dixon and Copenhagen, 1992). However, although AMPARs seem to be essential, NMDARs may play a lesser role, at least in transient ACs (Matsui et al, 2001;Vigh and Witkovsky, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Prolonged Reciprocal Signaling via NMDA and GABA Receptors at a Retinal Ribbon Synapse

Vı́gh

Gersdorff

2005

J. Neurosci.

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AMPA and GABA A receptors mediate most of the fast signaling in the CNS. However, the retina must, in addition, also convey slow and sustained signals. Given that AMPA and GABA A receptors desensitize quickly in the continuous presence of agonist, how are sustained excitatory and inhibitory signals transmitted reliably across retinal synapses? Reciprocal synapses between bipolar and amacrine cells in the retina are thought to play a fundamental role in tuning the bipolar cell output to the dynamic range of ganglion cells. Here, we report that glutamate release from goldfish bipolar cell terminals activates first AMPA receptors, followed by fast and transient GABA Amediated feedback. Subsequently, prolonged NMDA receptor activation triggers GABA A and a slow, sustained GABA C -mediated reciprocal inhibition. The synaptic delay of the NMDA/GABA C -mediated feedback showed stronger dependence on the depolarization of the bipolar cell terminal than the fast AMPA/GABA A -mediated response. Although the initial depolarization mediated by AMPA receptors was important to prime the NMDA action, NMDA receptors could trigger feedback by themselves in most of the bipolar terminals tested. This AMPA-independent feedback (delay Ϸ 10 ms) was eliminated in 2 mM external Mg 2ϩ and reduced in some terminals, but not eliminated, by TTX. NMDA receptors on amacrine cells with depolarized resting membrane potentials therefore can mediate the late reciprocal feedback triggered by continuous glutamate release. Our findings suggest that the characteristics of NMDA receptors (high agonist affinity, slow desensitization, and activation/deactivation kinetics) are well suited to match the properties of GABA C receptors, which thus provide part of the prolonged inhibition to bipolar cell terminals.

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Section: Discussionmentioning

confidence: 90%

Section: Complementary Properties Of Glutamate and Gaba Receptorsmentioning

confidence: 99%

Section: Desensitizing Ampars Trigger a Fast Gaba A Feedbackmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Prolonged Reciprocal Signaling via NMDA and GABA Receptors at a Retinal Ribbon Synapse

Vı́gh

Gersdorff

2005

J. Neurosci.

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“…TTX suppressed the light-evoked IPSCs, indicating that lateral inhibition depended on sodium action potentials. Figure 1B shows for a population of bipolar cells that TTX significantly and reversibly suppressed the charge transfer and peak amplitude of responses to light ON and to light OFF. Because amacrine cells express NMDA receptors, which are thought to amplify excitatory inputs (Dixon and Copenhagen 1992), the inclusion of D-AP5 in the control bath solution may have biased the system toward a greater reliance on action potentials to evoke transmitter release. Figure 1C shows that when D-AP5 was absent from the bath solution, TTX still reduced the light-evoked, ON and OFF IPSCs in bipolar cells but was slightly less effective.…”

Section: Light-evoked Gabaergic Ipscs In Bipolar Cells Depend On Actimentioning

confidence: 99%

Spike-Dependent GABA Inputs to Bipolar Cell Axon Terminals Contribute to Lateral Inhibition of Retinal Ganglion Cells

Shields

Lukasiewicz

2003

Journal of Neurophysiology

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The inhibitory surround signal in retinal ganglion cells is usually attributed to lateral horizontal cell signaling in the outer plexiform layer (OPL). However, recent evidence suggests that lateral inhibition at the inner plexiform layer (IPL) also contributes to the ganglion cell receptive field surround. Although amacrine cell input to ganglion cells mediates a component of this lateral inhibition, it is not known if presynaptic inhibition to bipolar cell terminals also contributes to surround signaling. We investigated the role of presynaptic inhibition by recording from bipolar cells in the salamander retinal slice. TTX reduced light-evoked GABAergic inhibitory postsynaptic currents (IPSCs) in bipolar cells, indicating that presynaptic pathways mediate lateral inhibition in the IPL. Photoreceptor and bipolar cell synaptic transmission were unaffected by TTX, indicating that its main effect was in the IPL. To rule out indirect actions of TTX, we bypassed lateral signaling in the outer retina by either electrically stimulating bipolar cells or by puffing kainate (KA) directly onto amacrine cell processes lateral to the recorded cell. In bipolar and ganglion cells, TTX suppressed laterally evoked IPSCs, demonstrating that both pre- and postsynaptic lateral signaling in the IPL depended on action potentials. By contrast, locally evoked IPSCs in both cell types were only weakly suppressed by TTX, indicating that local inhibition was not as dependent on action potentials. Our results show a TTX-sensitive lateral inhibitory input to bipolar cell terminals, which acts in concert with direct lateral inhibition to give rise to the GABAergic surround in ganglion cells.

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Distinct perisynaptic and synaptic localization of NMDA and AMPA receptors on ganglion cells in rat retina

Zhang

Diamond

2006

J of Comparative Neurology

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At most excitatory synapses, AMPA and NMDA receptors (AMPARs and NMDARs) occupy the postsynaptic density (PSD) and contribute to miniature excitatory postsynaptic currents (mEPSCs) elicited by single transmitter quanta. Juxtaposition of AMPARs and NMDARs may be crucial for certain types of synaptic plasticity, although extrasynaptic NMDARs also may contribute. AMPARs and NMDARs also contribute to evoked EPSCs in retinal ganglion cells (RGCs), but mEPSCs are mediated solely by AMPARs. Previous work indicates that an NMDAR component emerges in mEPSCs when glutamate uptake is reduced, suggesting that NMDARs are located near the release site but perhaps not directly beneath in the PSD. Consistent with this idea, NMDARs on RGCs encounter a lower glutamate concentration during synaptic transmission than do AMPARs. To understand better the roles of NMDARs in RGC function, we have used immunohistochemical and electron microscopic techniques to determine the precise subsynaptic localization of NMDARs in RGC dendrites. RGC dendrites were labeled retrogradely with cholera toxin B subunit (CTB) injected into the superior colliculus (SC) and identified using postembedding immunogold methods. Co-labeling with antibodies directed toward AMPARs and/ or NMDARs, we found that nearly all AMPARs are located within the PSD, while most NMDARs are located perisynaptically, 100-300 nm from the PSD. This morphological evidence for exclusively perisynaptic NMDARs localizations suggests a distinct role for NMDARs in RGC function.

show abstract

Two types of glutamate receptors differentially excite amacrine cells in the tiger salamander retina.

Cited by 97 publications

References 40 publications

Prolonged Reciprocal Signaling via NMDA and GABA Receptors at a Retinal Ribbon Synapse

Prolonged Reciprocal Signaling via NMDA and GABA Receptors at a Retinal Ribbon Synapse

Spike-Dependent GABA Inputs to Bipolar Cell Axon Terminals Contribute to Lateral Inhibition of Retinal Ganglion Cells

Distinct perisynaptic and synaptic localization of NMDA and AMPA receptors on ganglion cells in rat retina

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