PMID:15975715

Citation	Ide, S, Itoh, M and Goto, Y (2005) Defect in normal developmental increase of the brain biogenic amine concentrations in the mecp2-null mouse. Neurosci. Lett. 386:14-7
Abstract	To clarify whether Mecp2 dysfunction may cause impairment of the monoaminergic and serotonergic systems, we measured the whole brain concentrations of biogenic amines and related substrates in three mecp2-null male mice and four control mice of each age at 0-42 postnatal days by HPLC methods. After 14 postnatal days, concentrations of biogenic amines were smaller in mecp2-null mice than those in control mice and at 42 postnatal days, norepinephrine, dopamine and serotonin concentrations in mecp2-null mice were significantly smaller by 25, 24 and 16%, respectively. This result suggested that the absence of Mecp2 does not impair the neurogenesis of monoaminergic and serotonergic neurons but causes succeeding impairment of those neuronal systems from 14 postnatal days.
Links	PubMed Online version:10.1016/j.neulet.2005.05.056
Keywords	Animals; Animals, Newborn; Biogenic Monoamines/biosynthesis; Biogenic Monoamines/genetics; Brain/growth & development; Brain/metabolism; Brain Chemistry/genetics; Chromosomal Proteins, Non-Histone/genetics; DNA-Binding Proteins/genetics; Dopamine/biosynthesis; Female; Locus Coeruleus/metabolism; Locus Coeruleus/physiopathology; Male; Methyl-CpG-Binding Protein 2; Mice; Mice, Inbred C57BL; Mice, Knockout; Norepinephrine/biosynthesis; Raphe Nuclei/metabolism; Raphe Nuclei/physiopathology; Repressor Proteins/genetics; Rett Syndrome/metabolism; Rett Syndrome/physiopathology; Serotonin/biosynthesis
edit table

Annotations

Gene product	Qualifier	GO ID	GO term name	Evidence Code	with/from	Aspect	Notes	Status
edit table

References

See Help:References for how to manage references in GONUTS.