In the mid 1980s, the neuroactive steroids 3α,5α-tetrahydroprogesterone or allopregnanolone (3α,5α-THP) and 3α,5α- tetrahydrodeoxycorticosterone (3α,5α-THDOC) were shown to modulate neuronal excitability via their interaction with GABA A receptors. The steroids 3α,5α-THP and 3α,5α-THDOC were able to enhance the GABA-elicited Cl − current.  In addition, these steroids might enhance the binding of muscimol and benzodiazepines to GABA A receptors.  Structure- activity studies (SAR) showed that the 3alpha-OH group is essential for the anesthetic actions of these steroids,  they also have an optimally-placed hydrogen bond accepting group on the β face of the steroid at the C-17 position. The four steroid rings form a rigid framework for positioning these hydrogen groups in three-dimensional space.  Analogues 5 and 6 (Figure 10) are weak modulators of GABA A receptor function because the flexible side chains in these analogues do not have the conformations required for high biological activity. 
Sodium butyrate is a compound with formula Na(C 3 H 7 COO). It is the sodium salt of butyric acid . It has various effects on cultured mammalian cells including inhibition of proliferation , induction of differentiation and induction or repression of gene expression.  As such, it can be used in lab to bring about any of these effects. Specifically, butyrate treatment of cells results in histone hyperacetylation, and butyrate itself inhibits class I histone deacetylase (HDAC) activity,  specifically HDAC1 , HDAC2 , HDAC3 , and HDAC8 . Butyrate has been an essential vehicle for determining the role of histone acetylation in chromatin structure and function. Inhibition of HDAC activity is estimated to affect the expression of only 2% of mammalian genes.