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. Author manuscript; available in PMC: 2009 Oct 23.
Published in final edited form as: Neuron. 2008 Oct 23;60(2):343–352. doi: 10.1016/j.neuron.2008.10.002

Figure 4. Postsynaptic receptor desensitization and saturation do not affect short-term plasticity.

Figure 4

A, Example EPSC elicited by vestibular nerve stimulation in a YFP-16 neuron (black). Cyclothiazide (100 µm; gray) increased EPSC amplitude and slowed its decay, as is evident in the experimental trace peak-scaled to control (dotted line). B, No difference is seen in steady-state depression of synaptic currents in the presence of cyclothiazide at 50 Hz (shown) or other frequencies tested (n = 6). C, Summary of kinetics and steady-state depression across the population. The peak EPSC amplitude and the 80-20% decay time were both significantly increased by cyclothiazide (n = 6; p < 0.05). Steady-state depression, quantified as EPSC11-20/EPSC1, was unaffected. D, Example EPSC elicited in a YFP-16 neuron. γ-DGG (2 mM; gray) reduced EPSC amplitude without significantly affecting kinetics (scaled trace, dotted line). E, Reducing receptor saturation does not affect short-term depression at 50 Hz (shown) or other frequencies tested (n = 6). F, Summary of kinetics and steady-state depression across the population. EPSC amplitude was significantly reduced (p < 0.05) while other parameters were unaffected.