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Allopregnanolone (AP) is an endogenous neurosteroid.
The purpose of the present study was to evaluate the neuroendocrine effect of chlormadinone acetate (CMA) administration, analyzing the brain content of allopregnanolone (ALLO), an endogenous neurosteroid γ-aminobutyric acid agonist with anxiolytic properties, and the brain level of β-endorphin (β-END), an endogenous opioid implicated in pain mechanism, emotional state and autonomic control.
Deoxycorticosterone (DOC) is an endogenous neurosteroid present in the brain as well as in the peripheral circulation.
Deoxycorticosterone (DOC) is an endogenous neurosteroid found in brain and serum, precursor of the GABAergic neuroactive steroid (3α,5α -3,21-dihydroxypregnan-20-one (tetrahydrodeoxycorticosterone, THDOC) and the glucocorticoid corticosterone.
The anxiolytic actions of the endogenous neurosteroid 5α3α-THDOC were demonstrated almost 30 years ago (Crawley et al., 1986).
Non-benzodiazepines, such as etifoxine, are relatively safe for long-term use, and are known to increase endogenous neurosteroid levels (Verleye et al, 2005).
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These considerations have practical implications for actions of endogenous neurosteroids.
Endogenous neurosteroids and their synthetic analogs (neuroactive steroids) are potent modulators of GABAA receptors.
The endogenous neurosteroids, pregnenolone sulfate (PS) and 3α-hydroxy-5β-pregnan-20-one 3α-hydroxy-5β-pregnan-20-one 3α-hydroxy-5β-pregnan-20-one 3α-hydroxy-5β-pregnan-20-one 3α-hydroxy-5β-pregnan-20-one 3α-hydroxy-5β-pregnan-20-one
Of particular interest are endogenous neurosteroids that potently modulate the function of GABAARs and exhibit stress-protective properties.
As a corollary to this suggestion, modulation of GABAAR function by endogenous neurosteroids may be important in "fine tuning" HPA axis function.
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