Rett syndrome (RTT) is a severe neurodevelopmental disease caused by mutations 
in methyl-CpG-binding protein 2 (MECP2), which encodes a transcriptional 
modulator of many genes including BDNF. BDNF comprises nine distinct promoter 
regions, each triggering the expression of a specific transcript. The role of 
this diversity of transcripts remains unknown. MeCP2 being highly expressed in 
neurons, RTT was initially considered as a neuronal disease. However, recent 
studies have shown that MeCP2 was also expressed in astrocytes. Though several 
studies explored Bdnf IV expression in Mecp2-deficient mice, the differential 
expression of Bdnf isoforms in Mecp2-deficient neurons and astrocytes was never 
studied. By using TaqMan technology and a mouse model expressing a truncated 
Mecp2 (Mecp2(308/y)), we firstly showed in neurons that Bdnf transcripts 
containing exon I, IIb, IIc, IV, and VI are prominently expressed, whereas in 
astrocytes, Bdnf transcript containing exon VI is preferentially expressed, 
suggesting a specific regulation of Bdnf expression at the cellular level. 
Secondly, we confirmed the repressive role of Mecp2 only on the expression of 
Bdnf VI in neurons. Our data suggested that the truncated Mecp2 protein 
maintains its function on Bdnf expression regulation in neurons and in 
astrocytes. Interestingly, we observed that Bdnf transcripts (I and IXA), 
regulated by neural activity induced by bicuculline in Mecp2(308/y) neurons, 
were not affected by histone deacetylase inhibition. In contrast, Bdnf 
transcripts (IIb, IIc, and VI), regulated by histone deacetylation, were not 
affected by bicuculline treatment in wild-type and Mecp2(308/y) neurons. All 
these results reflect the complexity of regulation of Bdnf gene.