Figure 3. Fast-spiking GABAergic interneuron spike-timing-dependent plasticity.

A, schematic representation of STDP protocols and the corresponding raw traces of the postsynaptic GABAergic interneuron recording. An AP was evoked in the fast-spiking GABAergic interneuron a few milliseconds before (post-pre protocol) or after (pre-post protocol) a cortical stimulation (100 paired stimulations at 1 Hz). B, representative experiments of long-term plasticity induced by post-pre and pre-post protocols and EPSCs evoked in control (black) and 60 min after induction protocol (grey). Long-term synaptic efficacy changes were −63.7 ± 7.4% for LTD induced by post-pre protocol and +74.6 ± 11.7% for LTP induced by pre-post protocol (arrows indicate the induction protocols). C, STDP protocols induced bidirectional long-term synaptic plasticity (black triangles represent the mean ± s.e.m. of EPSC amplitude changes measured 60 min after induction protocol in 28 GABAergic interneurons). Post-pre protocols induced LTD for −40 < Δt < 0 ms (n = 10). Pre-post protocols induced LTP for 0 < Δt < +60 ms (n = 10). No long-term plasticity occurred for Δt < −40 ms and Δt > +60 ms (n = 8). Insets: normalized CV⁻² were plotted as a function of the normalized EPSC amplitude to determine the loci of the STDP. Mean variance analysis suggests that LTD has a mainly postsynaptic origin and LTP is mainly underlain by presynaptic mechanisms. Δt and induced plasticities were significantly correlated (r= 0.588, P < 0.01). This indicates a time-dependency of the STDP for GABAergic interneurons. D, histograms of EPSC amplitude changes. Histogram for post-pre protocols for −40 < Δt < 0 ms displayed a bimodal distribution fitted with a sum of two Gaussian functions, plotted individually, centred on 43.1 ± 1.2% and 97.3 ± 1.8% (n = 250 EPSCs, 10 GABAergic interneurons). This indicates the induction of either LTD (n = 9) or absence of plasticity (n = 1). Histogram for pre-post protocols for 0 < Δt < +60 ms displayed a unimodal distribution fitted with one Gaussian function centred on 141.1 ± 3.3% (n = 250 EPSCs, 10 GABAergic interneurons). This indicates that pre-post protocols induced LTP (n = 10). Histograms for post-pre and pre-post protocols for Δt < −40 ms and Δt > +60 ms displayed unimodal distributions fitted with one Gaussian function centred on 94.5 ± 2.8% for Δt < −40 ms (n = 100 EPSCs, 4 GABAergic interneurons) and 89.9 ± 2.4% for Δt > +60 ms (n = 100 EPSCs, 4 GABAergic interneurons), indicating an absence of long-term plasticity for both Δt.