Transporters buffer synaptically released glutamate on a submillisecond time scale:(缓冲synaptically释放谷氨酸转运蛋白的亚微秒级的时间尺度).pdfVIP
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Transporters buffer synaptically released glutamate on a submillisecond time scale:(缓冲synaptically释放谷氨酸转运蛋白的亚微秒级的时间尺度)
The Journal of Neuroscience, June 15, 1997, 17(12):4672–4687
Transporters Buffer Synaptically Released Glutamate on a
Submillisecond Time Scale
Jeffrey S. Diamond and Craig E. Jahr
The Vollum Institute, Oregon Health Sciences University, Portland, Oregon 97201
The role of transporters in clearing free glutamate from the The glutamate transient necessary to cause these effects was
synaptic cleft was studied in rat CA1 hippocampal neurons determined by developing a detailed kinetic model of the AMPA
cultured on glial microislands. The time course of free gluta- receptor. The model replicated the effects of KYN on the am-
mate in the cleft during a synaptic event was estimated by plitude and rise time of the synaptic responses when driven by
measuring the extent to which the rapidly dissociating AMPA glutamate transients that were similar to previous estimates
receptor antagonist kynurenate (KYN) was replaced by gluta- (Clements et al., 1992; Clements, 1996). The effects of THA
mate during a synaptic response. Dose inhibition of the AMPA were replicated by slowing and enlarging the slower phase of
receptor EPSC by KYN was less than predicted by the equilib- the dual component transient by about 20% or by prolonging
rium affinity of the antagonist, and the rise time of AMPA the single component by almost 40%. Because transport is too
receptor miniature EPSCs (mEPSCs) was slowed by KYN. Both
slow to account for these effects, it is concluded that transport-
results indicated that KYN dissociated from AMPA receptors
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