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. Author manuscript; available in PMC: 2010 Jul 16.
Published in final edited form as: Neuron. 2009 Jul 16;63(1):27–39. doi: 10.1016/j.neuron.2009.06.014

Figure 3. CNO effects on CA1 pyramidal neurons recorded in vitro.

Figure 3

Acute hippocampal slices were isolated from hM3Dq and control animals, and CA1 pyramidal cells were recorded from in the whole-cell configuration. Cells were held at resting membrane potential in the presence (A-B) or absence (C) of TTX, and CNO was bath applied. A, Bath application of CNO (500 nM) depolarized CA1 pyramidal cells from hM3Dq animals (i), but CNO did not affect resting membrane potential of CA1 pyramidal cells from control animals. However, bath application of carbachol (5 μM) did depolarize CA1 pyramidal cells from control animals (ii). Aiii, Population data from hM3Dq and control animals showing the mean resting membrane potential of CA1 pyramidal cells before and in the presence of CNO [500 nM for hM3Dq (n=7 cells from 5 animals) and 1 μM for control animals (n=7 cells from 5 animals)]. B, In the presence of an active PLC inhibitor (U73122, 10μM) the CNO-induced depolarization of hM3Dq CA1 pyramidal neurons was blocked (i), but in the presence of an inactive analog (U73343, 10μM) CNO was capable of depolarizing hM3Dq CA1 pyramidal neurons (ii). Biii, Population data showing change in resting membrane potential of hM3Dq CA1 pyramidal neurons induced by CNO (500nM) in the presence of U73122 (n=6 cells from 4 animals) or U73343 (n=4 cells from 4 animals). C, Bath application of CNO (500 nM) to hippocampal slices isolated from hM3Dq animals in the absence of TTX resulted in increased firing frequency and recurrent bursting.