Volume 27, Issue 1, Pages (July 2000)

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Volume 27, Issue 1, Pages 45-56 (July 2000) Timing-Based LTP and LTD at Vertical Inputs to Layer II/III Pyramidal Cells in Rat Barrel Cortex  Daniel E Feldman  Neuron  Volume 27, Issue 1, Pages 45-56 (July 2000) DOI: 10.1016/S0896-6273(00)00008-8

Figure 1 Physiology of Excitatory Vertical Synapses on Layer II/III Pyramidal Cells (A) Position of stimulation, recording, and bicuculline electrodes relative to barrels in layer IV during an experiment. (Inset) Biocytin-filled layer II pyramidal cell visualized by avidin-biotin-HRP histochemistry. (B1) Representative EPSCs recorded from three pyramidal cells in voltage clamp. Vhold = −70 mV. Bottom trace shows multicomponent EPSC. (B2) Representative EPSPs from three cells in current clamp (Vrest ≅ −75 mV). (C) Example of EPSC reversal at 0 mV. Holding potential is indicated. A slow NMDA receptor current was prominent at depolarized potentials. (D) AMPA and NMDA receptor components of the EPSC. A fast AMPA current, prominent at −90 mV, was blocked by 10 μM CNQX. In the same cell, a CNQX-resistant, slower NMDA receptor current was revealed by depolarization to +20 mV and was blocked reversibly by 50 μM D-APV. Traces are means of 20–30 sweeps. Neuron 2000 27, 45-56DOI: (10.1016/S0896-6273(00)00008-8)

Figure 2 LTP and LTD Induced in Voltage Clamp by Pairing Presynaptic Stimulation with Postsynaptic Depolarization (A) Experiment showing LTP. After a short baseline period (Vhold = −70 mV), the cell was depolarized to 0 mV for 50 stimuli without changing the stimulation rate. Points denote EPSC amplitude for each sweep of the experiment. LTP was apparent upon return to −70 mV as a stable increase in EPSC amplitude without significant changes in Rinput or Rseries. Dashed line, mean EPSC amplitude at the end of baseline. (Inset) Means of 50 EPSCs at the end of the baseline period and beginning 10 min after pairing. (B) Experiment demonstrating LTD. The protocol was identical to that in (A), except that the cell was depolarized to −50 mV for 100 sweeps to induce LTD. (C) Mean effect of pairing at 0 mV (eight cells, 50–100 pairing sweeps). Error bars, SEM. (D) Mean effect of pairing at −50 mV (eleven cells, 100 pairing sweeps). (E) Amount of LTP or LTD for each cell tested. Bars show mean, and error bars show SEM for each pairing condition. Neuron 2000 27, 45-56DOI: (10.1016/S0896-6273(00)00008-8)

Figure 3 LTP and LTD Induced by AP-EPSP Pairing (A1 and A2) Example of LTP. Points in A2 denote EPSP initial slope for each sweep (stimulation rate: 0.133 Hz). During pairing, an AP was elicited by somatic current injection (+1.1 nA, 5 ms) after each EPSP. The AP-EPSP delay was +3 ms (EPSP leading). After pairing, LTP was observed without changes in Rseries, Rinput, or Vm. Traces in A1 show average EPSPs for baseline period and a period beginning 10 min after pairing (50 sweeps each). The mean AP during pairing is also shown. Arrowheads indicate EPSP onset and AP peak. (Inset traces) Change in initial slope with LTP. (B1 and B2) Experiment demonstrating LTD. The protocol was identical to that in (A), except that the AP-EPSP delay during pairing was −107 ms (AP leading). (C–F) Mean effects of AP-EPSP pairing. (C) Pairing delays of +3 to +15 ms (EPSP leading, 75–100 pairing sweeps, n = 5 cells). Points show means for 1 min epochs. Error bars, SEM. (D) Pairing delays of −8 to −50 ms (AP leading, 100 pairing sweeps, n = 15 cells). (E) Control experiments in which only EPSPs (top, n = 5 cells) or only APs (bottom, n = 6 cells) were evoked during the “pairing” period. (F) Change in EPSP slope for all cells. Bars show mean ± SEM. Dashed line, no plasticity. Neuron 2000 27, 45-56DOI: (10.1016/S0896-6273(00)00008-8)

Figure 4 LTP and LTD Induced by Transient Changes in AP-EPSP Timing (A) Example of LTP. (A1) Top row, mean traces (50 sweeps each) showing EPSP, AP, and current pulse for measuring Rinput (asterisk) in different epochs of the experiment. Bottom row, EPSPs enlarged from the upper traces. (Inset traces) Initial slope of the EPSP before and after pairing, demonstrating LTP. (A2) EPSP initial slope during baseline and postpairing periods, when the AP-EPSP delay was +500 ms. During pairing, the AP-EPSP delay was shifted to +9 ms for 40 sweeps. (B) Example of LTD. The same protocol was used as in (A), except that during pairing, the AP-EPSP delay was shifted from +500 ms to −49 ms (AP leading) for 100 sweeps. (C) Mean effect of changing the AP-EPSP delay to +10 ms (40–100 sweeps, n = 6 cells). (D) Mean effect of changing the delay to −20 ms (100 sweeps, n = 7 cells). (E) Control experiments in which a +500 ms delay was maintained throughout the experiment. (F) Change in EPSP slope for each cell. Bars show mean ± SEM. Neuron 2000 27, 45-56DOI: (10.1016/S0896-6273(00)00008-8)

Figure 5 Temporal Windows for Induction of LTP and LTD by AP-EPSP Pairing (A) EPSP slope ratio for each cell tested, as a function of AP-EPSP delay during pairing. Triangles, standard AP-EPSP pairing protocol at 20°C–23°C. Closed circles, delay change protocol at 20°C–23°C. Squares, delay change protocol at 32° ± 1°C. Lines connect mean slope ratios for different ranges of pairing delays (see text). Δt > 0 indicates positive delays, and Δt < 0 indicates negative delays. Dashed lines, ±SEM for cells in control experiments (n = 16). (B) Mean EPSP slope ratio for the different ranges of pairing delays. Closed points show delays that produced EPSP slope ratios significantly different from those in control experiments. (C) Plasticity does not require disinhibition. Top, PSPs from representative cells with and without BMI (solid traces, Vm = −73 mV; dotted traces, Vm = −50 mV). With BMI, depolarization lengthened EPSPs, consistent with NMDA receptor activation, but revealed no IPSPs. Without BMI, depolarization often revealed early EPSPs followed by later, hyperpolarizing IPSPs. Bottom, effect of AP-EPSP pairing for all cells tested without BMI. Bars show mean ± SEM. (D) The long window for LTD induction is not due to blockade of AHPs by BMI. Top, BMI but not PTX reduces the mAHP in a representative cell. Traces are means of 10–15 sweeps. Bottom, AP-EPSP pairing at −50 ms delays induced significant LTD in the presence of both PTX and BMI. BMI data are from experiments in Figure 3 and Figure 4. Abbreviations: fAHP and mAHP, fast and medium AHPs following a single AP (truncated); Rec, recovery after BMI. Neuron 2000 27, 45-56DOI: (10.1016/S0896-6273(00)00008-8)

Figure 6 Depression of EPSPs Uncorrelated with Postsynaptic APs (A) Example of LTD induced by randomly varying AP-EPSP delays (range of delays: −50 to +50 ms). (A1) Five consecutive postsynaptic APs evoked during pairing, relative to the mean baseline and postpairing EPSPs. Dashed line, EPSP onset. (A2) Actual distribution of AP-EPSP delays during pairing for this cell, relative to the windows for LTP and LTD (from Figure 5). (A3) EPSP slope for each sweep of the experiment. Pairing with random delays induced LTD (EPSP slope ratio: 0.45). (B) Mean effect of pairing with random delays. Seven cells were tested with delays that varied randomly from −50 to +50 ms (closed circles), and five cells were tested with delays that varied from −10 to +10 ms (open circles). (Inset) Actual distribution of pairing delays across all cells for each group. Neuron 2000 27, 45-56DOI: (10.1016/S0896-6273(00)00008-8)

Figure 7 Model for Timing-Based LTP and LTD during Univibrissa Rearing Each panel shows two neighboring barrel columns in S1, representing adjacent whiskers. Only layers I–IV are shown. White ovals represent barrels in layer IV. Ticks on schematic axons represent hypothesized patterns of AP firing. (A) Univibrissa rearing. Vertical pathways in the deprived barrel column are assumed to be spontaneously active, and spontaneous activity is hypothesized to be poorly correlated with postsynaptic spiking and therefore to drive depression (minus sign) via the learning rule in Figure 5. (B) Normal whisker experience. All pathways show whisker-evoked activity. Firing of layer IV cells drives firing of layer II/III neurons in each column, resulting in small, positive AP-EPSP delays. Circled plus sign, hypothesized LTP. (C) All whiskers cut. All pathways are spontaneously active. Low firing rates in layer II/III are hypothesized to lead to fewer AP-EPSP pairings and therefore less LTD (small minus sign). See text for details. Neuron 2000 27, 45-56DOI: (10.1016/S0896-6273(00)00008-8)