Steroids, neuroactive steroids and neurosteroids in psychopathology

  title={Steroids, neuroactive steroids and neurosteroids in psychopathology},
  author={Bernardo O. Dubrovsky},
  journal={Progress in Neuro-Psychopharmacology and Biological Psychiatry},
  • B. Dubrovsky
  • Published 1 February 2005
  • Biology, Medicine
  • Progress in Neuro-Psychopharmacology and Biological Psychiatry
Potential use of neurosteroids and neuroactive steroids as modulators of symptoms of depression, anxiety, and psychotic disorders
It will be profitable to search for and establish symptom‐steroid relationships, as well as pharmacological and endogenous factors that can modulate NS biosynthesis and NAS formation, to be able to use these steroids in therapy.
Neurosteroids, neuroactive steroids, and symptoms of affective disorders
  • B. Dubrovsky
  • Psychology, Medicine
    Pharmacology Biochemistry and Behavior
  • 2006
Reconsidering Classifi cations of Depression Syndromes: Lessons from Neuroactive Steroids and Evolutionary Sciences
It is proposed that it would be more fruitful to focus on relationships between NAS and symptoms of psychiatric disorders, rather than with typologically defined disorders.
Neuroactive Steroids in Anxiety and Stress
Ten animal models of anxiety and stress are described that are significantly altered by one or more groups of neuroactive steroids and their interactions with stress-induced behaviors in experimental animals and humans are reviewed.
Neuroactive steroid regulation of neurotransmitter release in the CNS: Action, mechanism and possible significance
  • P. Zheng
  • Biology, Medicine
    Progress in Neurobiology
  • 2009
3α-reduced neuroactive steroids and their precursors during pregnancy and the postpartum period
Neuroactive steroids increased significantly from 10 to 36 weeks of pregnancy, except for 5β-DHP and PREGNEN which did not change significantly, and at 6 weeks postpartum all steroids were significantly reduced compared with late prenatal values.
Neuroactive Steroids and Related Steroids in Autism Spectrum Disorders
Future studies on levels of NASs in ASD should include careful consideration of the factors mentioned above, the possible advantages of saliva sampling and the use of assay procedures that provide simultaneous analysis of levels of a large number of these steroids.
Oxidative Stress-Mediated Brain Dehydroepiandrosterone (DHEA) Formation in Alzheimer’s Disease Diagnosis
The cumulative evidence for oxidative stress as a natural regulator of DHEA formation is presented and the use of this concept to develop a blood-based diagnostic tool for neurodegenerative diseases linked to oxidative stress, such as AD is developed.


  • E. Baulieu
  • Biology, Medicine
  • 1998
The neuropsychopharmacological potential of neuroactive steroids.
  • R. Rupprecht
  • Biology, Medicine
    Journal of psychiatric research
  • 1997
Selective serotonin reuptake inhibitors directly alter activity of neurosteroidogenic enzymes.
  • L. D. Griffin, S. Mellon
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 1999
The neurosteroid 3alpha-hydroxysteroid-5alpha-pregnan-20-one (allopregnanolone) acts as a positive allosteric modulator of gamma-aminobutyric acid at gamma-aminobutyric acid type A receptors and
Neuroactive steroids and anxiety disorders.
Diverse mechanisms for rapid steroid effects have now been described, and the nongenomic effects of NASs may involve γ-aminobutyric acid receptors, glutamate receptors, nicotinic acetylcholine receptors, sigma receptors, 5-HT3 receptors, or voltage- or non-voltage-gated calcium channels.
Potentiation of GABAergic Neurotransmission by Steroids
This chapter discusses a few selected areas related to the pharmacology, physiology, and chemistry of GABAergic neuroactive steroids, including their potential roles in alcohol dependence and withdrawal, as well as in affective disorders.
GABAA receptor α4 subunit suppression prevents withdrawal properties of an endogenous steroid
In this model, withdrawal of progesterone leads to increased seizure susceptibility and insensitivity to benzodiazepine sedatives through an effect on gene transcription, which is due to reduced levels of 3α,5α-THP which enhance transcription of the α4 subunit of the GABAA receptor.