Nicotinic receptor in dopamine neurons mediates learned odor choice.

Loss of the nicotinic acetylcholine receptor α1 subunit (Dα1) in Drosophila PAM dopamine neurons impairs appetitive odor-sugar associative memory and learned odor-choice performance.

• Why it matters: Nicotinic signaling is known to modulate dopaminergic output, but it was unclear how it supports the specific computations needed for odor choice during learning when cues compete.
• What they did: The authors tested nine nAChR genes and found Dα1 required in PAM neurons; they confirmed Dα1 expression and used live imaging to show reduced odor-evoked synaptic Caa2+ signals after Dα1 knockdown.
• The result: Dα1 knockdown preserved sugar-evoked Ca2+ responses yet reduced performance in a two-odor forced-choice discrimination task, with no deficit in single-odor pursuit or innate odor choice.

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