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• W2018224009 endingPage "637" @default.
• W2018224009 startingPage "625" @default.
• W2018224009 abstract "NMDA receptors are glutamate receptor ion channels that contribute to synaptic plasticity and are important for many forms of learning and memory. In the amygdala, NMDA receptors are critical for the acquisition, retention, and extinction of classically conditioned fear responses. Although the GluN2B subunit has been implicated in both the acquisition and extinction of conditioned fear, GluN2C-knockout mice show reduced conditioned fear responses. Moreover, D-cycloserine (DCS), which facilitates fear extinction, selectively enhances the activity of GluN2C-containing NMDA receptors. To further define the contribution of GluN2C receptors to fear learning, we infused the GluN2C/GluN2D-selective potentiator CIQ bilaterally into the basolateral amygdala (3, 10, or 30 μg/side) following either fear conditioning or fear extinction training. CIQ both increased the expression of conditioned fear 24 h later and enhanced the extinction of the previously conditioned fear response. These results support a critical role for GluN2C receptors in the amygdala in the consolidation of learned fear responses and suggest that increased activity of GluN2C receptors may underlie the therapeutic actions of DCS." @default.
• W2018224009 created "2016-06-24" @default.
• W2018224009 creator A5003402513 @default.
• W2018224009 creator A5009940078 @default.
• W2018224009 creator A5041161550 @default.
• W2018224009 creator A5052655254 @default.
• W2018224009 date "2013-09-06" @default.
• W2018224009 modified "2023-10-17" @default.
• W2018224009 title "Potentiation of GluN2C/D NMDA Receptor Subtypes in the Amygdala Facilitates the Retention of Fear and Extinction Learning in Mice" @default.
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• W2018224009 doi "https://doi.org/10.1038/npp.2013.241" @default.
• W2018224009 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3895240" @default.
• W2018224009 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24008353" @default.
• W2018224009 hasPublicationYear "2013" @default.
• W2018224009 type Work @default.

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