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. Author manuscript; available in PMC: 2012 Dec 15.
Published in final edited form as: Neuroscience. 2011 Aug 2;198:69–94. doi: 10.1016/j.neuroscience.2011.07.061

Fig. 5.

Fig. 5

SNr GABA neurons have a calcium-activated plateau potential. (A) A representative SNr GABA neuron exhibiting a plateau potential that manifests as a prolonged membrane depolarization following a depolarizing current pulse delivered while the neuron is held hyperpolarized (black trace). The plateau potential is abolished in calcium-free conditions (red trace). (B) Another SNr GABA neuron exhibits a plateau potential under control conditions (black trace) that is abolished by nimodipine (10 µM; red trace) indicating the involvement of L-type calcium channels in plateau potential generation. (C) A SNr GABA neuron without a plateau potential under control conditions (black trace) is made to exhibit a plateau potential after activation of L-type calcium channels with Bay K 8644 (5 µM; red trace). (D) The plateau potential (black trace) is abolished in low-sodium conditions (red trace) suggesting that the conductance underlying the plateau potential is a calcium-activated nonselective cation conductance. (E) The plateau potential observed under control conditions (black trace) is abolished by the TRP channel blocker flufenamic acid (FFA; 200 µM; red trace). (F) A neuron not exhibiting a plateau potential under control conditions (black trace) exhibits a plateau potential in the presence of Bay K 8644 (blue trace). The evoked plateau potential is similarly abolished by FFA (red trace). Modified from Lee and Tepper, 2007b with permission. Copyright 2007 Society for Neuroscience.

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