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      Drosophila SLC22A transporter is a memory suppressor gene that influences cholinergic neurotransmission to the mushroom bodies

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      Neuron

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          SUMMARY

          The mechanisms that constrain memory formation are of special interest because they provide insights into the brain’s memory management systems and potential avenues for correcting cognitive disorders. RNAi knockdown in the Drosophila mushroom body neurons (MBn) of a newly discovered memory suppressor gene, Solute Carrier DmSLC22A, a member of the organic cation transporter family, enhances olfactory memory expression, while overexpression inhibits it. The protein localizes to the dendrites of the MBn, surrounding the presynaptic terminals of cholinergic afferent fibers from projection neurons (Pn). Cell-based expression assays show that this plasma membrane protein transports cholinergic compounds with the highest affinity among several in vitro substrates. Feeding flies choline or inhibiting acetylcholinesterase in Pn enhances memory; an effect blocked by overexpression of the transporter in the MBn. The data argue that DmSLC22A is a memory suppressor protein that limits memory formation by helping to terminate cholinergic neurotransmission at the Pn:MBn synapse.

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          Author and article information

          Journal
          8809320
          1600
          Neuron
          Neuron
          Neuron
          0896-6273
          1097-4199
          31 March 2016
          14 April 2016
          4 May 2016
          04 May 2017
          : 90
          : 3
          : 581-595
          Affiliations
          Department of Neuroscience, The Scripps Research Institute Florida, Jupiter, Florida 33458, USA
          Author notes
          Corresponding author: Ronald L. Davis, Department of Neuroscience, The Scripps Research Institute Florida, Jupiter, Florida 33458, USA, 561-228-3463, rdavis@ 123456scripps.edu
          [*]

          These authors made equal contributions

          Article
          PMC4894652 PMC4894652 4894652 nihpa773146
          10.1016/j.neuron.2016.03.017
          4894652
          27146270
          1063246f-5ee6-4be4-917f-93e3ff05811c
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          2017-12-12 12:38 UTC
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