G. I. Wilkie

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The modulation of [3H]ACh release by nicotinic compounds was studied in superfused rat hippocampal synaptosomes loaded with [3H]choline. (−)-Nicotine (0.1–10 μM) evoked a dose-dependent increase in [3H]ACh release; higher concentrations were less effective. Nicotine-evoked release was Ca2+-dependent, and blocked by the nicotinic antagonists(More)
The effects of the nicotinic agonist (+)-anatoxin-a have been examined in four different preparations, representing at least two classes of neuronal nicotinic receptors. (+)-Anatoxin-a was most potent (EC50 = 48 nM) in stimulating 86Rb+ influx into M10 cells, which express the nicotinic receptor subtype comprising alpha 4 and beta 2 subunits. A presynaptic(More)
Introduction Nicotine promotes transmitter release in the brain by a direct action on presynaptic terminals. Pharmacological evidence confirms that this action is mediated by nicotinic acetylcholine receptors (nAChR). The most abundant brain nAChR, the a4B2 subtype, is identified by the binding of tritiated nicotine ([,H]Nic) [ 13. Lesioning and subcellular(More)
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