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. 2018 Oct 25;7:e38588. doi: 10.7554/eLife.38588

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© 2018, Dorman et al

This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.

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Figure 6. — (A) Attenuation of spine calcium elevation by inhibition is timing-dependent. GABAergic stimulation attenuates the spine calcium elevation evoked by coordinated glutamatergic stimulation when GABAergic stimulation occurs between 25 ms before to 50 ms after glutamateric stimulation for fast GABA_A kinetics, or 100 ms before to 50 ms after glutamatergic stimulation for slow GABA_A kinetics. The GABAergic synapse was located on the dendritic shaft at the same location as clustered glutamatergic stimulation of 16 distally located neighboring spines. (B) Attenuation of spine calcium elevation by inhibition is location-dependent. GABAergic stimulation simultaneous with glutamatergic stimulation (of 16 distal, neighboring spines) attenuates supralinear spine calcium elevation when the GABAergic stimulation is located distally, near the clustered glutamatergic stimulation, whereas single proximal GABAergic synaptic inputs have little effect. For both A-B, peak spine calcium is normalized to the no-GABA control, and fast (diamonds) or slow (squares) GABA_A kinetics correspond to GABA_A synapses from SPNs, LTSIs, FSIs (fast), or NGFs (slow). (C) Strong proximal inhibitory input, corresponding to FSIs, enhances supralinear spine calcium elevation for sub- or near-threshold stimulations (16 spines per branch on one or two branches). The peak calcium elevation in all stimulated spines is shown as box-and-whisker plots. The effect of inhibition (GABA; red bars) on peak spine calcium in stimulated spines is higher than control (gray bars) for 16 spines per branch (left) but not 32 spines per branch (right). Both excitatory and inhibitory synapses were stimulated during the same time frame in these simulations. Figure 6—figure supplement 1 shows the peak spine calcium vs. dendritic location for each stimulated spine.

Figure 6—figure supplement 1. — (A) Attenuation of spine calcium elevation by inhibition is timing-dependent. GABAergic stimulation attenuates the spine calcium elevation evoked by coordinated glutamatergic stimulation when GABAergic stimulation occurs between 25 ms before to 50 ms after glutamateric stimulation for fast GABA_A kinetics, or 100 ms before to 50 ms after glutamatergic stimulation for slow GABA_A kinetics. The GABAergic synapse was located on the dendritic shaft at the same location as clustered glutamatergic stimulation of 16 distally located neighboring spines. (B) Attenuation of spine calcium elevation by inhibition is location-dependent. GABAergic stimulation simultaneous with glutamatergic stimulation (of 16 distal, neighboring spines) attenuates supralinear spine calcium elevation when the GABAergic stimulation is located distally, near the clustered glutamatergic stimulation, whereas single proximal GABAergic synaptic inputs have little effect. For both A-B, peak spine calcium is normalized to the no-GABA control, and fast (diamonds) or slow (squares) GABA_A kinetics correspond to GABA_A synapses from SPNs, LTSIs, FSIs (fast), or NGFs (slow). (C) Strong proximal inhibitory input, corresponding to FSIs, enhances supralinear spine calcium elevation for sub- or near-threshold stimulations (16 spines per branch on one or two branches). The peak calcium elevation in all stimulated spines is shown as box-and-whisker plots. The effect of inhibition (GABA; red bars) on peak spine calcium in stimulated spines is higher than control (gray bars) for 16 spines per branch (left) but not 32 spines per branch (right). Both excitatory and inhibitory synapses were stimulated during the same time frame in these simulations. Figure 6—figure supplement 1 shows the peak spine calcium vs. dendritic location for each stimulated spine.