ArticleJournal of neurodevelopmental disorders2025
GABAergic regulation of Locus coeruleus activity in necdin-deficient mice, an animal model of Prader-Willi syndrome.
Article in Journal of neurodevelopmental disorders, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPrader-Willi syndrome (PWS) is a neurodevelopmental disorder caused by loss of paternally expressed genes on chromosome 15q11-13, including NDN, which encodes necdin. Necdin deficiency has been linked to impaired visuospatial memory, social recognition, and stress regulation-features also seen in PWS. Previous work showed that necdin-deficient (Ndn + m/-p) mice exhibit reduced activity of noradrenergic neurons in the locus coeruleus (LC), a nucleus essential for arousal and stress responses. However, the mechanisms underlying LC hypoactivity remain unclear. Because GABAergic signaling is critical for LC excitability, this study examined the role of GABA
methodsElectrophysiological recordings from brainstem slices of wild-type (WT) and Ndn + m/-p mice were used to measure spontaneous firing rates (SFRs) of LC noradrenergic neurons. The effects of bicuculline (GABA
resultsLC-NE neurons in Ndn + m/-p mice exhibited significantly reduced baseline SFR compared with WT. Bicuculline did not alter firing in either genotype, whereas CGP54626 significantly increased SFR in WT but not in Ndn + m/-p neurons, indicating impaired GABA
conclusionNecdin deficiency selectively disrupts GABA
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