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Figure 3 | Molecular Pain

Figure 3

From: Inhibitory coupling between inhibitory interneurons in the spinal cord dorsal horn

Figure 3

GABA A R- and glycine receptor-mediated mIPSCs in Lamina II inhibitory neurons. A. Recordings of mIPSCs in presence of 1 μM TTX at a holding potential of 0 mV using CsMeSO3-filled micropipettes. mIPSC frequency was 0.38 ± 0.06 Hz (n = 9). The traces on the left show mIPSCs in control conditions (top and middle), displaying different decay kinetics, and in the presence of strychnine (bottom) displaying only slow decay kinetics. The traces on the right are averages of 100 consecutive mIPSCs in control (top) and in the presence of strychnine (bottom). Administration of strychnine abolished the fastest component of the complex decay kinetics of the average mIPSCs confirming that this component was mediated by glycine receptors as previously established [26, 27]. Inset: Histogram showing the distribution of GABAAR-mediated mIPSC decay τ in the presence of strychnine. B. Three individual mIPSCs showing characteristic different decay kinetics: fast decay (left; absent in strychnine thus presumably glycinergic); slow decay (middle; GABAA-mediated); mixed fast and slow (both glycine and GABAA-mediated). The proportion of fast, slow or mixed mIPSCs varied across cells. Fast decaying mIPSC proportions ranged from 17% to 93%, slow decaying mIPSCs from 5% to 78% and mixed mIPSCs from 1% to 10%. Five out of nine neurons showed predominately (> 70%) fast mIPSCs, two out of nine were having predominately (> 70%) slow mIPSCs. C. Cumulative probability plot of the slow mIPSC decay τ (black) and the decay τ of the slow component from mixed mIPSCs (red), no significant difference between the two populations was found (p > 0.05; Kolmogorov-Smirnov test). All recordings we performed in the presence of 10 μM CNQX and 40 μM APV.

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