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Dissecting the machinery of nicotine's reward

in mice lacking the ß2 subunit showed no response to nicotine compared to normal mice, in which nicotine enhanced the neurons' firing. However, mice lacking the a7 subunit did show a neuronal response to nicotine, although it was not the same response as in normal mice.

The researchers confirmed the importance of the ß2 subunit by using a harmless virus to reintroduce it back into the mice lacking it. They found that reintroduction in a specific region of the brain (the ventral tegmental area; VTA) was sufficient to restore the normal neuronal nicotine response. A prior study also showed that mice lacking the ß2 subunit also showed reduced exploratory behavior, which was also restored when the researchers added the subunit back. This finding thus showed that the dopaminergic brain circuitry was involved in such behaviors as curiosity or interest in novelty, wrote the researchers.

The researchers concluded that their "data suggest that a concomitant activation of [ß2 and a7 receptor subunits] may be a necessary requirement for the full expression of the sequence of events leading to nicotine reinforcement."

The researchers said that the findings "are consistent with the suggestion of a hierarchical role of the two subunits." While the ß2 subunit would mediate a "global tonic" regulation of dopamine-producing neurons by nicotine and acetylcholine, the a7 subunit would more finely tune the response of these neurons, they concluded.


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Source:Cell Press


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