MeCP2 is abundantly expressed in the mature brain specifically in the hypothalamus and can either repress or activate gene expression [30], [31]. It has also been implicated in the behavioral response of rodents to drugs of abuse. For example, Im et al., 2010 [32] showed that knockdown of MeCP2 in the dorsal striatum decreased rat's intake of cocaine and implicated MeCP2 in the compulsive response of rats to this drug. Furthermore, they showed that cocaine stimulation of MeCP2 decreased the expression of miR-212 and miR-132 resulting in an increase of BDNF expression with an increase in cocaine intake. Moreover, MeCP2 has been implicated in stress regulation. Fyffe et al., 2008 [33] showed that MeCP2 knockout in the hypothalamus of mice resulted in specific behavioral phenotypes such as increased aggression, anxiety, abnormal response to stress and hyperphagia which are also endophenotypes observed in fetal-alcohol exposed rodents and human subjects [2], [34]. MeCP2 regulates chromatin structure of several genes and modulates their expression [30], [32]. We have previously shown that fetal alcohol exposure increases DNA methyltransferases (Dnmt)1 and the histone repressive mark
