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. 2014 Dec 1;171(24):5790–5801. doi: 10.1111/bph.12880

Figure 2.

Figure 2

4-bromopropofol, but not propofol, significantly decreased the discharge rate of ventral horn neurons by opening glycine receptors. In each individual experiment, action potential activity was normalized to the firing rate observed under drug-free control conditions. A normalized activity of 100% indicates that the tested drugs did not alter the discharge rate as compared with the pre-drug condition. A normalized activity of 0% stands for the total depression of action potential firing. The graph shows that 50 nM propofol (PRO; n = 30) did not decrease action potential firing as compared with sham-treated slices (n = 57). Contrastingly, 4-bromopropofol (BP) reduced neuronal activity by about 30% (n = 31). 4-bromopropofol was similarly effective in the presence and absence of the specific GABAA receptor antagonist bicuculline (80 μM, n = 33), indicating that 4-bromopropofol did not act via GABAA receptors. In the presence of the specific glycine antagonist strychnine (1 μM, n = 35), 4-bromopropofol failed to reduce action potential firing, indicating that the drug acted via glycine receptors. **P < 0.01, significantly different from sham; anova. Numbers of experiments are shown as insets in the columns.