Roles of glial glutamate transporters in shaping EPSCs at the climbing fiber-Purkinje cell synapses

Takatsuru, Yusuke; Takayasu, Yukihiro; Iino, Masae; Nikkuni, Osamu; Ueda, Yuto; Ozawa, Seiji

doi:10.1016/j.neures.2005.11.002

Cited by 31 publications

(40 citation statements)

References 37 publications

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“…The application of 200 nM PMB-TBOA, which inhibited glial glutamate transporters almost completely with a minor effect on neuronal ones (Takatsuru et al, 2006), caused slow-rising CF-EPSCs in WT mice, whose properties were similar to those of atypical CF-EPSCs in GLAST-deficient mice. Our results suggest that the atypical CF-EPSCs in GLAST-deficient mice are generated by a low concentration of glutamate released from neighboring CFs.…”

Section: Introductionmentioning

confidence: 87%

“…1 A, top traces). The application of 200 nM PMB-TBOA prolonged the weighted decay time constant of these conventional CF-EPSCs significantly in WT mice because of the retarded removal of synaptically released glutamate attributable to the lack of function of glial glutamate transporters (Takatsuru et al, 2006). However, this treatment exerted no influence on either rise time or peak amplitude of these CF-EPSCs.…”

Section: Slow-rising Cf-epscs Under Conditions In Which Glial Glutamamentioning

confidence: 92%

“…PMB-TBOA was shown to inhibit STCs evoked by CF stimulation in Bergmann glia in mice in a dose-dependent manner with the IC 50 value of 46.9 nM. The bath application of 200 nM PMB-TBOA suppressed STCs in Bergmann glia in mice almost completely, whereas it reduced STCs evoked by CF stimulation in PCs only by 9.6% (Takatsuru et al, 2006). In this study, we obtained similar results in Bergmann glia and PCs in cerebellar slices of young rats (P13-P17) (see supplemental Fig.…”

Section: Inhibition Of Glial Glutamate Transporters By Pmb-tboamentioning

confidence: 92%

“…PMB-TBOA at 200 nM inhibited both GLAST and GLT1 almost completely (Shimamoto et al, 2004), whereas GLT1 on Bergmann glia remains functional in GLAST-deficient mice (Takatsuru et al, 2006). Therefore, the removal of released glutamate would be retarded more severely by the application of 200 nM PMB-TBOA than in the mutant mice.…”

Section: Glutamate Spillovermentioning

confidence: 97%

“…It has been shown that the suppression of glial glutamate transporters by 200 nM PMB-TBOA prolonged the decay of fastrising CF-EPSCs (Takatsuru et al, 2006). This decay prolonged by PMB-TBOA was markedly speeded by lowering the extracellular Ca 2ϩ concentration.…”

Section: Lowering Glutamate Release Probability Preferentially Reducementioning

confidence: 99%

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Glial Glutamate Transporters Maintain One-to-One Relationship at the Climbing Fiber-Purkinje Cell Synapse by Preventing Glutamate Spillover

Takayasu

Iino

Shimamoto

et al. 2006

Journal of Neuroscience

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A glial glutamate transporter, GLAST, is expressed abundantly in Bergmann glia and plays a major role in glutamate uptake at the excitatory synapses in cerebellar Purkinje cells (PCs). It has been reported that a higher percentage of PCs in GLAST-deficient mice are multiply innervated by climbing fibers (CFs) than in the wild-type (WT) mice, and that CF-mediated EPSCs with small amplitude and slow rise time, designated as atypical slow CF-EPSCs, are observed in these mice. To clarify the mechanism(s) underlying the generation of these atypical CF-EPSCs, we used (2S,3S)-3-[3-(4-methoxybenzoylamino)benzyloxy]aspartate (PMB-TBOA), an inhibitor of glial glutamate transporters. After the application of PMB-TBOA, slow-rising CF-EPSCs were newly detected in WT mice, and their rise and decay kinetics were different from those of conventional fast-rising CF-EPSCs but similar to those of atypical CF-EPSCs in GLAST-deficient mice. Furthermore, both slow-rising CF-EPSCs in the presence of PMB-TBOA in WT mice and atypical CF-EPSCs in GLAST-deficient mice showed much greater paired-pulse depression compared with fast-rising CF-EPSCs. In addition, both of them were more markedly inhibited by ␥-D-glutamyl-glycine, a low-affinity competitive antagonist of AMPA receptors. These results indicated that both of these types of EPSCs were mediated by a low concentration of glutamate released from neighboring CFs. Based on all of these findings, we suggest that glial transporters prevent glutamate released from a single CF from spilling over to neighboring PCs other than the synaptically connected PC, and play an essential role in the maintenance of the functional one-to-one relationship between CFs and PCs.

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Section: Introductionmentioning

confidence: 87%

Section: Slow-rising Cf-epscs Under Conditions In Which Glial Glutamamentioning

confidence: 92%

Section: Inhibition Of Glial Glutamate Transporters By Pmb-tboamentioning

confidence: 92%

Section: Glutamate Spillovermentioning

confidence: 97%

Section: Lowering Glutamate Release Probability Preferentially Reducementioning

confidence: 99%

See 3 more Smart Citations

Glial Glutamate Transporters Maintain One-to-One Relationship at the Climbing Fiber-Purkinje Cell Synapse by Preventing Glutamate Spillover

Takayasu

Iino

Shimamoto

et al. 2006

Journal of Neuroscience

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The mother of turf wars: Carotid stents

White¹

2004

Cathet Cardio Intervent

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Morphogenesis and regulation of Bergmann glial processes during Purkinje cell dendritic spine ensheathment and synaptogenesis

Lippman

Lordkipanidze

Buell

et al. 2008

Glia

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Astrocytes have an important role in synaptic formation and function but how astrocytic processes become associated with synaptic structures during development is not well understood. Here we analyzed the pattern of growth of the processes extending off the main Bergmann glial (BG) shafts during synaptogenesis in the cerebellum. We found that during this period BG process outgrowth was correlated with increased ensheathment of dendritic spines. In addition, two-photon time-lapse imaging revealed that BG processes were highly dynamic, and processes became more stable as the period of spine ensheathment progressed. While process motility was dependent on actin polymerization, activity of cytoskeletal regulators Rac1 and RhoG did not play a role in glial process dynamics or density, but was critical for maintaining process length. We extended this finding to probe the relationship between process morphology and ensheathment, finding that shortened processes result in decreased coverage of the spine. Furthermore, we found that areas in which BG expressed dn-Rac1, and therefore had a lower level of synaptic ensheathment, showed an overall increase in synapse number. These analyses reveal how BG processes grow to surround synaptic structures, elucidate the importance of BG process structure for proper development of synaptic ensheathment, and reveal a role for ensheathment in synapse formation.

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Roles of glial glutamate transporters in shaping EPSCs at the climbing fiber-Purkinje cell synapses

Cited by 31 publications

References 37 publications

Glial Glutamate Transporters Maintain One-to-One Relationship at the Climbing Fiber-Purkinje Cell Synapse by Preventing Glutamate Spillover

Glial Glutamate Transporters Maintain One-to-One Relationship at the Climbing Fiber-Purkinje Cell Synapse by Preventing Glutamate Spillover

The mother of turf wars: Carotid stents

Morphogenesis and regulation of Bergmann glial processes during Purkinje cell dendritic spine ensheathment and synaptogenesis

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