ArticleExperimental & molecular medicine2025
GluN2B-mediated regulation of silent synapses for receptor specification and addiction memory.
Article in Experimental & molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- Increased NMDAR activity and GluN2A-NMDAR silent synapse expansion induced by chronic benzodiazepine treatment.Neuropharmacology · 2025Article
- The mesolimbic reward pathway is necessary for disruptions in cocaine-seeking behavior following mediated devaluation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Resource-dependent heterosynaptic spike-timing-dependent plasticity in recurrent networks with and without synaptic degeneration.Frontiers in computational neuroscience · 2025Article
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12 authors.
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Abstract
Psychostimulants, including cocaine, elicit stereotyped, addictive behaviors. The reemergence of silent synapses containing only NMDA-type glutamate receptors is a critical mediator of addiction memory and seeking behaviors. Despite the predominant abundance of GluN2B-containing NMDA-type glutamate receptors in silent synapses, their operational mechanisms are not fully understood. Here, using conditional depletion/deletion of GluN2B in D1-expressing accumbal medium spiny neurons, we examined the synaptic and behavioral actions that silent synapses incur after repeated exposure to cocaine. GluN2B ablation reduces the proportion of silent synapses, but some of them can persist by substitution with GluN2C, which drives the aberrantly facilitated synaptic incorporation of calcium-impermeable AMPA-type glutamate receptors (AMPARs). The resulting precocious maturation of silent synapses impairs addiction memory but increases locomotor activity, both of which can be normalized by the blockade of calcium-impermeable AMPAR trafficking. Collectively, GluN2B supports the competence of cocaine-induced silent synapses to specify the subunit composition of AMPARs and thereby the expression of addiction memory and related behaviors.
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