Bicuculline methiodide potentiates NMDA-dependent burst firing in rat dopamine neurons by blocking apamin-sensitive Ca2+-activated K+ currents
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Acknowledgements
This study was funded by PHS grant MH40416. We wish to thank B. Anna McCoy for her helpful comments.
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2016, Handbook of Behavioral NeuroscienceCitation Excerpt :Local application of bicuculline methiodide produced a modest but statistically significant 25% increase in firing rate (Paladini and Tepper, 1999; Tepper et al., 1995). Two other GABAA antagonists that do not block the SK channel (as does bicuculline methiodide, Johnson and Seutin, 1997), PTX and gabazine, exerted smaller, less consistent excitatory effects on firing rate (Paladini and Tepper, 1999). Local application of the selective GABAB receptor antagonists, 2-OH-saclofen or CGP55845A, exerted even more modest, but opposite effects on firing rate, producing small decreases in spontaneous activity (Paladini and Tepper, 1999; Tepper et al., 1995).
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2014, Handbook of Clinical NeurologyDisruption of Dopamine Neuron Activity Pattern Regulation through Selective Expression of a Human KCNN3 Mutation
2013, NeuronCitation Excerpt :Dopamine neurons do not typically exhibit spontaneous burst activity in slice (Shepard and Bunney, 1991; Overton and Clark, 1997; Wolfart et al., 2001; Wolfart and Roeper, 2002; Hopf et al., 2007). However, bath application of NMDA can occasionally lead to burst firing in dopamine neurons (Johnson et al., 1992; Johnson and Wu, 2004), which is enhanced by pharmacological suppression of SK currents (Seutin et al., 1993; Johnson and Seutin, 1997). To determine the extent to which hSK3Δ facilitates NMDAR-mediated burst firing in slice, we recorded spontaneous action potentials in GFP- and hSK3ΔGFP-expressing neurons after bath application of NMDA (20 μM).