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Figure 5 | Molecular Pain

Figure 5

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

Figure 5

Propofol-potentiated IPSCs are mediated by GABA A receptor chloride channels. A: GABAA IPSCs were evoked in a VB relay neuron in a horizontal slice by RTN stimulation (50 μA, 180 μs, every 15 s) in the presence of the GABAB antagonist 2-OH saclofen (100 μM). The membrane potential was clamped at -60 mV. Synaptic currents were potentiated by propofol (3 μM, 10 min). Overlay showing current amplitude in the absence (control) and presence of propofol. Each trace is an average of 10 sweeps. B: normalized traces showing that propofol prolonged the decay time of IPSCs. C: propofol-potentiated eIPSCs could be abolished by picrotoxin (100 μM). D-F: bar graphs of pooled data indicate that propofol increased eIPSC amplitude, decay time, and charge transfer in a concentration-dependent manner. *: P < 0.05, one-way ANOVA, vs. control, n = 20.

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Molecular Pain

ISSN: 1744-8069

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