ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2018
Genetic loss of GluN2B in D1-expressing cell types enhances long-term cocaine reward and potentiation of thalamo-accumbens synapses.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 9 citations in OpenAlex.
- Dopamine D2 receptors bypass canonical signaling to directly tune NMDA receptor function and aversive learning.Science advances · 2026Article
- Identification of photoperiod as a regulator of dopamine-mediated behavior in female mice.Neurobiology of sleep and circadian rhythms · 2025Article
- A Cocaine-Activated Ensemble Exerts Increased Control Over Behavior While Decreasing in Size.Biological psychiatry · 2025Article
- D1 and D2 medium spiny neurons in the nucleus accumbens core have distinct and valence-independent roles in learning.Neuron · 2024Article
- Neuropeptide Y modulates excitatory synaptic transmission and promotes social behavior in the mouse nucleus accumbens.Neuropharmacology · 2022Article
- Kappa opioid receptor modulation of excitatory drive onto nucleus accumbens fast-spiking interneurons.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Cannabinoid type 1 receptors in A2a neurons contribute to cocaine-environment association.Psychopharmacology · 2021Article
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4 authors at 1 institution in 1 country.
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Abstract
Transient upregulation of GluN2B-containing NMDA receptors (R) in the nucleus accumbens (NAc) is proposed as an intermediate to long-term AMPAR plasticity associated with persistent cocaine-related behaviors. However, cell type- and input-specific contributions of GluN2B underlying lasting actions of cocaine remain to be elucidated. We utilized GluN2B cell type-specific knockouts and optogenetics to deconstruct the role of GluN2B in cocaine-induced NAc synaptic and behavioral plasticity. While reward learning was unaffected, loss of GluN2B in D1 dopamine receptor-expressing cells (D1) led to prolonged retention of reward memory. In control mice, prefrontal cortex (PFC)-D1(+) NAc AMPAR function was unaffected by cocaine exposure, while midline thalamus (mThal)-D1(+) NAc AMPAR function was potentiated but diminished after withdrawal. In D1-GluN2B
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