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. Author manuscript; available in PMC: 2021 Jan 1.
Published in final edited form as: J Neuroendocrinol. 2019 Sep 30;32(1):e12792. doi: 10.1111/jne.12792

Figure 2. Diagram of the hypothesized role of neurosteroids in the neurobehavioral complications induced by sleep deprivation.

Figure 2.

Similar to other stressors, acute sleep deprivation leads to increased expression of 5-alpha reductase and synthesis of the neurosteroid allopregnanolone in the PFC. Whereas this upregulation is likely aimed at counterbalancing the detrimental impact of oxidative stress induced by sleep deprivation, such compensatory mechanism may in turn set off neurobehavioral complications by interfering with the corticolimbic connections responsible for executive functions and emotional regulation. Enzymes: CYP21A2: Steroid 21-hydroxylase; 3β-HSD; 3β-hydroxysteroid dehydrogenase; 3α-HSOR: 3α-hydroxysteroid oxidoreductase. Steroids: DOC, deoxycorticosterone; 5α-DHDOC, 5α-dihydro deoxycorticosterone; 3α,5α-THDOC, 3α,5α-tetrahydrodeoxycorticosterone, DHP, 5α-dihydroprogesterone. See text for further details.