The Journal of Neuroscience, September 6, 2006, ():
The Activation of Excitatory Glutamate Receptors Evokes a Long-Lasting Increase in the Release of GABA from Cerebellar Stellate Cells
J. Neurosci. Liu and Lachamp
26: 9332
Supplemental data
Files in this Data Supplement:
- supplemental material
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Fig 1. Glycine potentiates the extrasynaptic NMDAR current. (A) The peak current amplitude. (B) Total charge transfer (normalized to the control value). (C) Average current traces prior to, during and following the application of 20 μM glycine. (D) Mean amplitude of NMDAR-mediated currents increased during the application of glycine (n = 5; p < 0.02). (E) Average total charge transfer increased during glycine application (n = 5; p < 0.03). (F) Decay time constant remained unchanged during the application of glycine (p = 0.16).
Methods: The current mediated by extrasynaptic NMDARs was measured using coronal slices in a whole cell-voltage clamp configuration. Pipettes were filled with a Cs+-based BAPTA solution (in mM: 130 CsCl, 10 HEPES, 10 BAPTA, 5 TEACl, 5 QX314, 2 Na2ATP, 2 MgATP, 0.3 Na3GTP, 0.5 CaCl2). Parallel fibres were stimulated with four stimuli at 100 Hz every 30 second. The stimulating electrode was placed in the molecular layer about > 100 μm from the recorded cell. The stimulus intensity ranged from 18-50 V with a duration of 0.14-0.2 ms. The current was measured at +40 mV in the presence of NBQX (10 μM), picrotoxin (100 μM) and strychnine (1 μM) to block non-NMDA, GABAA and glycine receptors, respectively.
- supplemental material
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Fig 2. The spontaneous inhibitory synaptic current was mediated by GABAA receptors. Spontaneous synaptic currents were recorded in the presence of 5 μM NBQX and 0.3 μM TTX. This current was blocked by SR-95531.
