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. 2003 Mar 21;548(Pt 3):731–743. doi: 10.1113/jphysiol.2002.035998

Figure 7. Effect of hypoxia, halothane and AA on the membrane potential and excitability in GPN neurones.

Figure 7

Representative examples of the hypoxia-induced membrane depolarisation and action potential firing in GPN neurones during current-clamp recordings are shown in A (left) and B, respectively. The histogram in A (right) shows that hypoxia (Hox) caused a significant (**P < 0.001) decrease of the resting potential to −46.8 ± 1.6 mV from −49.8 ± 1.6 mV (n = 18) during normoxia (Nox). C, representative example of the response to hypoxia before, during, and after application of halothane (Hal, 2–5 mm). Note that halothane caused membrane depolarisation and occlusion of the hypoxic response. D, representative example of the effect of AA (5 μm) on the resting potential. Note that AA caused a long-lasting hyperpolarisation and its effects were poorly reversible. In the example, recovery of the resting potential was reached ∼30 min after AA was removed from the extracellular solution.