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Results We demonstrate a developmental perturbation in CCK-expressing excitatory neurons within the mPFC: their density increases sharply in early postnatal life, stabilizes during adolescence, and typically declines in adulthood in wild-type (WT) mice, yet remains persistently elevated in adult KI counterparts
The development of specific inhibitors of these enzymes would be a very promising therapeutic strategy
The current understanding of progesterone's effects on NADPH supply and mitochondrial dysfunction relies partially on non-myomatous cell models
