Neurosteroids anxiety

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]

In a comparative study on 189 patients with adjustment disorder with anxiety, one group of patients took 150mg of Stresam daily for 28 days, while the other group took 2mg of Lorazepam (Ativan). The treatment efficiency was similar for both drugs regarding mean HAM-A score. However, more people from etifoxine group responded to the treatment by the day 28 (72% and 56%). The first group also experienced fewer side effects compared to lorazepam group and fewer cases of rebound anxiety. Similar results were obtained in the comparative study of Stresam with Alprazolam (Xanax).

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Neurosteroids anxiety

neurosteroids anxiety

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