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Figure 4 | Molecular Pain

Figure 4

From: Propofol suppresses synaptic responsiveness of somatosensory relay neurons to excitatory input by potentiating GABAA receptor chloride channels

Figure 4

Propofol suppresses trans -ACPD-evoked tonic spike firing in VB neurons. A: bath application of the metabotropic glutamate receptor agonist trans-ACPD (100 μM), which can mimic corticothalamic excitatory transmission [63], induced a sustained, tonic spike firing pattern (top). Addition of propofol (3 μM) depressed firing (middle), accompanied by spontaneous IPSPs (sIPSPs). The suppression could be blocked by bicuculline (10 μM; bottom). B: segments marked with "i, ii, iii" in A are expanded to view sIPSPs. Spikes are truncated for clarity. Note that few sIPSPs are seen prior to propofol application (i), small sIPSPs (< 6.5 mV, ii) and large sIPSPs (6.5 – 16.5 mV, iii) are observed following propofol application. Scale: 20 mV, 200 ms for i, 20 mV, 100 ms for ii and iii. C: time course histogram for group data (n = 8) showing propofol suppression of trans-ACPD-induced tonic spike firing rate. Arrows indicate the onset and duration of propofol application at given concentrations. The suppression of propofol could be blocked by bicuculline. SE bars (0.5 – 2.2) are omitted for clarity. D: bar graph of cumulative data indicates that propofol (prop) hyperpolarized the membrane potential (MP) and this effect was reversed during addition of bicuculline (+bic). *: P < 0.01, one way ANOVA with Tukey test, propofol vs. control, propofol vs. propofol + bicuculline. n = 8 – 12/each.

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