Journal: Journal of Neurophysiology

Article Title: Nicotine inhibits potassium currents in Aplysia bag cell neurons

doi: 10.1152/jn.00816.2015

Figure Lengend Snippet: Antagonist profile for the nicotine-evoked response at −10 mV. Shown are responses to 10 s of pressured-applied 3 mM nicotine (Nic) in cultured bag cell neurons under whole cell voltage-clamp at a −10 mV holding potential (HP) in nASW with K+-based internal solution. A, top: in control, the response evoked by the first nicotine application was very similar to that produced 10 min later by the second application (bottom). Because there was no desensitization, antagonists were evaluated by delivering drug during the intervening period and measuring any change between the initial and latter response. Scale bars apply to both traces. B: in a separate neuron, bath delivery of 100 μM mecamylamine, a nicotinic receptor blocker, did not alter the second response evoked by pressure-applied nicotine. Scale bars apply to both traces. C: summary data showing the percentage of remaining current between the second and first nicotine applications. None of the classical nicotinic receptor blockers, i.e., mecamylamine (mec), α-conotoxin ImI (ImI), or hexamethonium (hex), significantly altered the magnitude of the nicotine-evoked response (ordinary ANOVA). Numbers in bars indicate number of neurons.

Article Snippet: In some experiments, nASW, nicotine, or the structurally similar agonist, epibatidine ( Badio and Daly 1994 ), was continuously pressured-applied for 10 s. Drugs were made up as stock solutions in water, frozen at −20°C, and then diluted down to a working concentration in the extracellular or intracellular solutions as needed: nicotine (N0257; Sigma-Aldrich), mecamylamine hydrochloride (M9020; Sigma-Aldrich), α-conotoxin ImI (3119; Tocris Bioscience), hexamethonium dichloride (H2138; Sigma-Aldrich), (±)-epibatidine dihydrochloride hydrate (E1145; Sigma-Aldrich).

Techniques: Cell Culture, Produced