Functional correlation between allopregnanolone and [35S]‐TBPS binding in the brain of rats exposed to isoniazid, pentylenetetrazol or stress
Open accessAbstract
The relation between changes in the cerebral cortical concentration of allopregnanolone and γ‐aminobutyric acid (GABA) type A receptor function after intracerebroventricular injection of this neurosteroid was investigated in male rats. Intracerebroventricular administration of allopregnanolone (1.25 to 15 μg) produced a maximal increase (100 fold at the highest dose) in cortical allopregnanolone concentration within 5 min; the concentration remained significantly increased at 15 and 30 min, before returning to control values by 60 min. The same treatment induced a rapid and dose‐dependent decrease in the binding of t‐[35 S]‐butylbicyclophosphorothionate ([35 S]‐TBPS) to cerebral cortical membranes measured ex vivo, an effect mimicked by the benzodiazepine midazolam but not by the 3β‐hydroxyepimer of allopregnanolone. The time course of changes in [35 S]‐TBPS binding paralleled that of brain allopregnanolone concentration. In a dose‐dependent manner, allopregnanolone both delayed the onset of convulsions and inhibited the increase in [35 S]‐TBPS binding to cortical membranes induced by isoniazid. The potency of allopregnanolone in inhibiting [35 S]‐TBPS binding in isoniazid‐treated rats was approximately four times that in control animals. The ability of allopregnanolone to decrease [35 S]‐TBPS binding in isoniazid‐treated rats also correlated with its anticonvulsant activity against pentylenetetrazol‐induced seizures as well as its inhibitory effect on the increase in [35 S]‐TBPS binding induced by foot shock. The results indicate that the in vivo administration of allopregnanolone enhances the function of GABA A receptors in rat cerebral cortex and antagonizes the inhibitory action of stress and drugs that reduce GABAergic transmission.
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Allopregnanolone's interaction with GABAA receptors contributes to its anxiolytic, neuroprotective, neuromodulatory, and anti-gonadotropic properties.
“ALLO interaction with GABAA receptors contributes to ALLO’s anxiolytic, neuroprotective, neuromodulatory, and anti-gonadotropic properties66–68.”
From Emerging insights into hypothalamic‐pituitary‐gonadal axis regulation and interaction with stress signalling (2018) · cites this paper as [67]
The Introduction (p. 1) and Discussion (p. 6) say allopregnanolone enhances GABAA receptor function and report a prior finding of anxiolytic effects, supporting the anxiolytic and neuromodulatory parts of the claim. The passages do not link that interaction to neuroprotective or anti-gonadotropic properties; the Discussion’s general mention of sexual functions does not establish an anti-gonadotropic effect. (LLM, conf=0.87)
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- Authors
- Concas, A., Mostallino, M. C., Perra, C., Lener, R., Roscetti, G., Barbaccia, M. L., Purdy, R. H., & Biggio, G.
- Affiliations
- University of Cagliari (IT)
- University of Rome Tor Vergata (IT)
- University of California San Diego (US)
- Corresponding author
- Concas, Alessandra
- ORCID
- Venue
- British Journal of Pharmacology
- Publisher
- Wiley
- Published
- 1996-06
- Volume
- 118
- Issue
- 4
- Pages
- 839-846
- ISSN
- 0007-1188 (ISSN-L)
- 1476-5381
- PMC
- PMC1909514
- OpenAlex
- W2051790390
- Cited by
- 53
- References
- 49
- Citations by year
- 2022: 1 · 2018: 2 · 2016: 1 · 2015: 3 · 2014: 1 · 2013: 2 · 2012: 1
- FWCI
- 2.16
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- British Journal of Pharmacology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pharmacological Receptor Mechanisms and Effects
- Keywords
- allopregnanolone, GABAA receptor, [35S]TBPS binding, cerebral cortex, isoniazid, pentylenetetrazole, convulsions, anticonvulsant activity, stress, footshock, benzodiazepines, midazolam, neurosteroids, GABAergic neurotransmission
- MeSH terms
- Animals, Antitubercular Agents, Cerebral Cortex, Convulsants, Injections, Intraventricular, Isoniazid, Male, Pentylenetetrazole, Pregnanolone, Receptors, GABA-A, Seizures, Stress, Physiological, Time Factors, Rats, Sprague-Dawley, GABA Modulators, Bridged Bicyclo Compounds, Heterocyclic, Rats
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