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. Author manuscript; available in PMC: 2012 Aug 11.
Published in final edited form as: Neuron. 2011 Aug 11;71(3):488–497. doi: 10.1016/j.neuron.2011.06.012

Figure 3. POMC-hrGFP neuron depolarization by mCPP is not mediated by the inhibition of GIRK channels.

Figure 3

(A) Voltage clamp recordings of membrane currents at a holding potential of −40 mV. TTX (0.5 μM) was present in the bath solution throughout the recording. Successive application of baclofen (50 μM) elicited outward GIRK currents with similar amplitudes. (B) Pretreatment with mCPP prior to the second application of baclofen significantly reduced the second GIRK amplitudes. (C) Bar graph summarizing the averaged ratio of first and second GIRK current amplitudes (I2/I1). Data are presented in mean ± SEM and ** indicates P<0.01. Note that GABAB-activated GIRK currents are almost completely blocked by CGP54626 (2 μM). (D) Bath application of CGP54626 (2 μM) failed to affect the membrane potential of 9 POMC-hrGFP neurons tested. (E) mCPP depolarized some POMC-hrGFP neurons from GIRK1 knockout mice. Continuous recordings were interrupted to apply current step pulses as indicated (arrows) (a). mCPP decreased voltage deflections in response to hyperpolarizing current steps as shown at the bottom (b). Current versus voltage (I–V) plot from same neuron illustrating a characteristic decrease in input resistance subsequent to mCPP application. Shown are responses before (control) and during mCPP application. Note that the input resistance was decreased by mCPP (c).