Agis-balboa and neurosteroids

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. [13] In addition, these steroids might enhance the binding of muscimol and benzodiazepines to GABA A receptors. [30] Structure- activity studies (SAR) showed that the 3alpha-OH group is essential for the anesthetic actions of these steroids, [31] 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. [32] 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. [33]

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. [1] 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, [2] 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. [3]

Agis-balboa and neurosteroids

agis-balboa and neurosteroids

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