Abstract：
:Exposures to cocaine and morphine produce similar adaptations in nucleus accumbens (NAc)-based behaviors, yet produce very different adaptations at NAc excitatory synapses. In an effort to explain this paradox, we found that both drugs induced NMDA receptor-containing, AMPA receptor-silent excitatory synapses, albeit in distinct cell types through opposing cellular mechanisms. Cocaine selectively induced silent synapses in D1-type neurons, likely via a synaptogenesis process, whereas morphine induced silent synapses in D2-type neurons via internalization of AMPA receptors from pre-existing synapses. After drug withdrawal, cocaine-generated silent synapses became 'unsilenced' by recruiting AMPA receptors to strengthen excitatory inputs to D1-type neurons, whereas morphine-generated silent synapses were likely eliminated to weaken excitatory inputs to D2-type neurons. Thus, these cell type-specific, opposing mechanisms produced the same net shift of the balance between excitatory inputs to D1- and D2-type NAc neurons, which may underlie certain common alterations in NAc-based behaviors induced by both classes of drugs.
journal_name
Nat Neuroscijournal_title
Nature neuroscienceauthors
Graziane NM,Sun S,Wright WJ,Jang D,Liu Z,Huang YH,Nestler EJ,Wang YT,Schlüter OM,Dong Ydoi
10.1038/nn.4313subject
Has Abstractpub_date
2016-07-01 00:00:00pages
915-25issue
7eissn
1097-6256issn
1546-1726pii
nn.4313journal_volume
19pub_type
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