Developmental Changes in AMPA and Kainate Receptor-Mediated Quantal Transmission at Thalamocortical Synapses in the Barrel Cortex

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  Figure 1.
Figure 1.

Extracellular Sr2+ desynchronizes release at thalamocortical synapses in developing barrel cortex. A, Low-power infrared DIC image of the barrel cortex in a thalamocortical slice in the recording chamber. Scale bar, 100 μm. B, High-power infrared DIC image of a neuron in barrel cortex during a patch-clamp recording. Scale bar, 10 μm. C, Biocytin-filled cell in layer IV neonatal barrel cortex. Scale bar, 10 μm. For A-C, pial surface is located toward the top. D, Example EPSCs (single traces) evoked by stimulation in ventrobasal thalamus collected during a whole-cell patch-clamp recording from a layer IV neuron in the barrel cortex in the presence of normal extracellular solution (2.5 mm Ca2+, 0 mm Sr2+; left) and in the presence of 4 mm Sr2+ (2 mm EGTA, 0 mm Ca2+; right). Insets show averaged EPSCs from the same cell evoked by paired-pulse stimulation. E, Example experiment (same cell as in D) showing EPSC amplitude (percentage of baseline before application of Sr2+) versus time for an experiment in which 4 mm Sr2+ (2 mm EGTA, 0 mm Ca2+) was applied extracellularly. F, Summary data from 14 cells showing the reduction in EPSC amplitude with Sr2+ application. G, Summary data from eight cells showing the change in paired-pulse ratio (EPSC2/EPSC1) with Sr2+.

  1. The Journal of Neuroscience vol. 25 no. 21 5259-5271
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