1. Timing and Specificity of Feed-Forward Inhibition within the LGN
Dawn M. Blitz, Wade G. Regehr 
Neuron 
Volume 45, Issue 6, Pages (March 2005)
DOI: /j.neuron
Copyright © 2005 Elsevier Inc. Terms and Conditions

2. Figure 1
EPSCs and IPSCs Have Identical Stimulus Intensity Thresholds in a Subset of TC Neurons
(A) A schematic of the slice preparation illustrates recording and stimulation locations. Abbreviations: dLGN, dorsal lateral geniculate nucleus; vLGN, ventral lateral geniculate nucleus. (B) Example recordings of synaptic currents elicited by RGC activation at the same stimulus intensity, but recorded at three different holding potentials, are shown. Each trace is the average of five trials. The regions of the synaptic currents used for analysis and the corresponding symbols are shown above the traces in (B). (C) Voltage dependence of the amplitudes of the EPSC (closed circles) and IPSC (open circles) elicited by RGC activation. Each point is the average of five trials from the cell shown in (B). (D and F) EPSC and IPSC amplitudes are plotted as a function of stimulus intensity (HP = −10 mV). Averages of five trials recorded just before (1) and just after (2) reaching EPSC threshold are shown above each graph. Stimulus artifacts have been blanked for clarity in all traces. (E and G) Schematics are shown to illustrate the likely circuitry underlying results in (D) and (F). T = 36–38°C.
Neuron  , DOI: ( /j.neuron )
Copyright © 2005 Elsevier Inc. Terms and Conditions

3. Figure 2
In a Subset of TC Neurons, Inhibition Is Locked to Activation of Individual RGC Inputs
The holding potential was set at −10 mV to enable identification of both IPSCs and EPSCs, the stimulus intensity was set to elicit ∼50% failures of EPSCs, and many trials were recorded for two neurons. In the first of these neurons (A–E), there was no apparent link between the occurrence of the EPSC and the size of the IPSC, as is seen by considering all of the trials (A), the trials in which the EPSC failed to occur (B), the trials in which the EPSC was observed (C), the average of the failures (gray), and the average of the successes (black) (D), or by plotting the IPSC amplitude against EPSC amplitude for all trials (E). In the second neuron (F–J), a similar analysis reveals that inhibition is tightly locked to the excitation. Stimulus artifacts have been blanked for clarity. Vertical arrows indicate time of stimulus. Scale bars in (C) and (H) are for (A)–(C) and (F)–(H), respectively. T = 36–38°C.
Neuron  , DOI: ( /j.neuron )
Copyright © 2005 Elsevier Inc. Terms and Conditions

4. Figure 3
Summary of TC Neurons with Inhibition that Is Locked and Not Locked to Activation of Individual RGC Inputs
The IPSC amplitude is plotted as a function of EPSC amplitude at the threshold of EPSC activation for failures and successes of the EPSC (A and B). Neurons are separated into “nonlocked” ([A], n = 51) and “locked” ([B], n = 29) EPSC/IPSC combinations, using criteria that are described in the text. The changes in IPSC amplitude when EPSC thresholds were crossed are plotted as cumulative histograms (C) for 80 neurons.
Neuron  , DOI: ( /j.neuron )
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5. Figure 4
Locked IPSCs Provide Short-Latency Inhibition while Nonlocked IPSCs Exhibit a Wide Range of Latencies
(A and B) EPSC/IPSC combinations recorded at two stimulus intensities are shown for two example nonlocked neurons. Thick traces were elicited at lower stimulus intensities than were thin traces. Traces are the average of 15 (A) and 50 trials (B). T = 35°C (A) and 36°C (B). The latency from EPSC to IPSC onset in locked neurons was determined in two ways, as demonstrated for the same cell (C–F). First, GABAA and AMPA components were isolated at reversal potentials for AMPA (top, 10 mV) and for GABAA (bottom, −60 mV) (C), and then the conductances were determined (D). Second, currents arising from both AMPA and GABAA components were measured at −10 mV; then the AMPA component was measured in isolation in the presence of picrotoxin (20 µM), and the GABAA component was determined by subtraction (E). These two methods gave similar results (D and F). Traces in (C) and (E) are the averages of 15 trials, T = 38°C. Latencies are indicated by dashed vertical lines. (G) Summary of latencies measured as a function of temperature for 14 neurons. In four neurons, latency measurements were made at multiple temperatures. Closed symbols indicate latencies calculated using the method shown in (C); open symbols indicate latencies measured using the method shown in (E). A line of the form y = a + bx was fit to all the data points; a = 6.5, b = −0.14. (H) Latencies measured at 37–38.5°C in seven neurons are plotted in histogram form.
Neuron  , DOI: ( /j.neuron )
Copyright © 2005 Elsevier Inc. Terms and Conditions

6. Figure 5
Locked IPSCs Are Depressed to a Greater Extent than Nonlocked IPSCs during Physiological Activity Patterns
(A and B) Recordings of nonlocked (A) and locked (B) IPSCs during a train in four example neurons are shown. Vertical bars above the recordings indicate the stimulus pattern. In each case, a single IPSC is overlaid for comparison (gray traces). Neurons were held at the reversal potential for the EPSC (10 mV). Traces are the average of 6–18 trials. Stimulus artifacts have been blanked for clarity. (C) The amplitudes of the 2nd through the 6th IPSC normalized to the first IPSC in the train are plotted for nonlocked (open circles, n = 5) and locked (closed circles, n = 7) inhibition. (D) The ratios of the amplitudes of the 2nd to the 1st IPSC are plotted for nonlocked (open circles, n = 7) and locked (closed circles, n = 5) inhibition with interstimulus intervals of 10 ms to 4 s. (E) The normalized amplitudes of the 5th IPSC during regular trains of 10–100 Hz frequency are plotted for nonlocked (open circles, n = 5) and locked (closed circles, n = 4) inhibition. Data in (C)–(E) are plotted as the mean (±SEM). Significant differences between locked and nonlocked IPSCs are indicated with asterisks (*p < 0.05, Student’s t test).
Neuron  , DOI: ( /j.neuron )
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7. Figure 6
Dynamic Clamp Experiments Indicate that Locked Inhibition Has Little Influence on TC Neuron Responses in Burst Mode
(A) The AMPA, NMDA, and GABAA conductance waveforms used in dynamic-clamp experiments are plotted. (B–D) Example recordings (B), raster plots (C), and average histograms (D) of responses to injection of simulated AMPA (40 nS) and NMDA (30 nS) conductances in the absence (left) and presence (right) of a 10 nS GABA conductance are shown for an example experiment. The average numbers of action potentials per bin (1 ms) per trial (50) are plotted. (E) The average numbers of action potentials elicited during the train are plotted for trials with 0 nS, 5 nS, or 10 nS GABA conductances with 40/30 nS AMPA/NMDA (closed circles) and 30/20 nS AMPA/NMDA (open circles) conductances (n = 4). The decreases in spike number at 5 nS GABA for 40/30 nS AMPA/NMDA and at 5 nS and 10 nS GABA for 30/20 nS AMPA/NMDA were significant relative to 0 nS GABA (p < 0.05, paired Student’s t test). The data in (E) are plotted as the mean (±SEM). Vertical bars above the recordings and the plots indicate the stimulus pattern.
Neuron  , DOI: ( /j.neuron )
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8. Figure 7 Locked Inhibition Alters TC Neuron Responses in Tonic Mode
Dynamic-clamp experiments were performed as in Figure 6, but the initial membrane potential corresponded to tonic mode (∼−55 mV). Recordings (A), raster plots (B), and average histograms (C) are shown for an example experiment. Data from individual trials (A), 50 randomized trials (B), and the average of 50 trials (C) illustrate the responses to 40/30 nS AMPA/NMDA conductances in the absence (left) and presence (right) of a 10 nS GABA conductance. Vertical bars above the recordings and the plots indicate the stimulus pattern.
Neuron  , DOI: ( /j.neuron )
Copyright © 2005 Elsevier Inc. Terms and Conditions

9. Figure 8
In Tonic Mode, Locked Inhibition Improves Precision and Decreases Multiple Spikes per Stimulus
Experiments performed as in Figure 7 are summarized for six cells. (A) The average number of action potentials elicited by 40/30 nS AMPA/NMDA conductances in the absence (left) and presence (right) of a 10 nS GABA conductance are plotted per bin (1 ms) per trial (50). (B) The average numbers of action potentials per train are plotted for trials with 0 nS, 5 nS, or 10 nS GABA conductances with 40/30 nS AMPA/NMDA (closed circles) and 30/20 nS AMPA/NMDA (open circles) conductances. The decreases in spike number were significant at each conductance combination relative to 0 nS GABA (p < 0.01, paired Student’s t test). The data are plotted as the mean (±SEM). (C) The timing of action potentials between the first and second stimuli in the train are plotted as average histograms for 40/30 nS AMPA/NMDA conductances in the absence (left) and presence (right) of a 10 nS GABA conductance. The late component (3–8 ms) was significantly reduced (p < 0.05, paired Student’s t test). (D) The fraction of trials that had one (black bars) or two or more (white bars) spikes between the first and second stimuli are plotted for 0 nS, 5 nS, and 10 nS GABA conductances for 30/20 nS AMPA/NMDA (left) and 40/30 nS AMPA/NMDA (right) conductance combinations. All of the changes in the fraction of trials with one or two or more spikes for 5 nS and 10 nS GABA compared to 0 nS GABA were significant (p < 0.05, paired Student’s t test). The data are plotted as the mean (±SEM).
Neuron  , DOI: ( /j.neuron )
Copyright © 2005 Elsevier Inc. Terms and Conditions