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- W2302214910 abstract "The modern diet has become highly sweetened, resulting in unprecedented levels of sugar consumption, particularly among adolescents. While chronic long-term sugar intake is known to contribute to the development of metabolic disorders including obesity and type II diabetes, little is known regarding the direct consequences of long-term, binge-like sugar consumption on the brain. Because sugar can cause the release of dopamine in the nucleus accumbens (NAc) similarly to drugs of abuse, we investigated changes in the morphology of neurons in this brain region following short- (4 weeks) and long-term (12 weeks) binge-like sucrose consumption using an intermittent two-bottle choice paradigm. We used Golgi-Cox staining to impregnate medium spiny neurons (MSNs) from the NAc core and shell of short- and long-term sucrose consuming rats and compared these to age matched water controls. We show that prolonged binge-like sucrose consumption significantly decreased the total dendritic length of NAc shell MSNs compared to age-matched control rats. We also found that the restructuring of these neurons resulted primarily from reduced distal dendritic complexity. Conversely, we observed increased spine densities at the distal branch orders of NAc shell MSNs from long-term sucrose consuming rats. Combined, these results highlight the neuronal effects of prolonged binge-like intake of sucrose on NAc shell MSN morphology." @default.
- W2302214910 created "2016-06-24" @default.
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- W2302214910 date "2016-03-23" @default.
- W2302214910 modified "2023-09-24" @default.
- W2302214910 title "Prolonged Consumption of Sucrose in a Binge-Like Manner, Alters the Morphology of Medium Spiny Neurons in the Nucleus Accumbens Shell" @default.
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- W2302214910 doi "https://doi.org/10.3389/fnbeh.2016.00054" @default.
- W2302214910 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4803740" @default.
- W2302214910 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27047355" @default.
- W2302214910 hasPublicationYear "2016" @default.
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