ArticleThe Journal of physiology2005
Neurosteroid administration and withdrawal alter GABAA receptor kinetics in CA1 hippocampus of female rats.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- Catamenial-like seizure exacerbation in mice with targeted ablation of extrasynaptic δGABA-a receptors in the brain.Journal of neuroscience research · 2017Article
- Role of GABAMolecular brain · 2017Review
- Article
- Pubertal Expression of α4βδ GABAA Receptors Reduces Seizure-Like Discharges in CA1 Hippocampus.Scientific reports · 2016Article
- Altered γ-aminobutyric acid neurotransmission in major depressive disorder: a critical review of the supporting evidence and the influence of serotonergic antidepressants.Drug design, development and therapy · 2015Review
- Perimenstrual-like hormonal regulation of extrasynaptic δ-containing GABAA receptors mediating tonic inhibition and neurosteroid sensitivity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Characterization of neurosteroid effects on hyperpolarizing current at α4β2δ GABAA receptors.Psychopharmacology · 2014Article
- Neurosteroid interactions with synaptic and extrasynaptic GABA(A) receptors: regulation of subunit plasticity, phasic and tonic inhibition, and neuronal network excitability.Psychopharmacology · 2013Review
- A mouse kindling model of perimenstrual catamenial epilepsy.The Journal of pharmacology and experimental therapeutics · 2012Article
- Knockout of the γ-aminobutyric acid receptor subunit α4 reduces functional δ-containing extrasynaptic receptors in hippocampal pyramidal cells at the onset of puberty.Brain research · 2012Article
- Estrous cycle and stress: influence of progesterone on the female brain.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2012Article
- Developmental Coordination of Gene Expression between Synaptic Partners During GABAergic Circuit Assembly in Cerebellar Cortex.Frontiers in neural circuits · 2012Article
- Diagnosis and management of catamenial seizures: a review.International journal of women's health · 2012Article
- Role of anticonvulsant and antiepileptogenic neurosteroids in the pathophysiology and treatment of epilepsy.Frontiers in endocrinology · 2011Article
- Article
- Stoichiometry of expressed alpha(4)beta(2)delta gamma-aminobutyric acid type A receptors depends on the ratio of subunit cDNA transfected.The Journal of biological chemistry · 2010Article
- Trace and contextual fear conditioning is enhanced in mice lacking the alpha4 subunit of the GABA(A) receptor.Neurobiology of learning and memory · 2010Article
- Puberty, steroids and GABA(A) receptor plasticity.Psychoneuroendocrinology · 2009Article
- Chronic exposure to anabolic androgenic steroids alters neuronal function in the mammalian forebrain via androgen receptor- and estrogen receptor-mediated mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Neurosteroid replacement therapy for catamenial epilepsy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2009Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Withdrawal from the GABA-modulatory steroid 3alpha-OH-5alpha-pregnan-20-one (3alpha,5alpha-THP) following exposure of female rats to the parent compound progesterone (P) produces a syndrome characterized by behavioural excitability in association with up-regulation of the alpha4 subunit of the GABA(A) receptor (GABAR) in the hippocampus. Similar changes are seen after 48 h exposure to its stereoisomer, 3alpha,5beta-THP. Here, we further characterize the effects of P withdrawal on GABAR kinetics, using brief (1 ms) application of 5-10 mm GABA to outside-out patches from acutely isolated CA1 hippocampal pyramidal cells. Under control conditions, GABA-gated current deactivated biexponentially, with tau(fast) = 12-19 ms (45-60% of the current), and tau(slow) = 80-140 ms. P withdrawal resulted in marked acceleration of deactivation (tau(fast) = 3-7 ms and tau(slow) = 30-100 ms), as did 48 h exposure to 3alpha,5beta-THP (tau(fast) = 5-8 ms; tau(slow) = 40-120 ms). When recombinant receptors were tested in HEK-293 cells, a similar acceleration in tau(fast) was observed for alpha4beta2delta and alpha4beta2gamma2 GABARs, compared to alpha1beta2gamma2 and alpha5beta2gamma2 receptors. In addition, tau(slow) was also accelerated for alpha4beta2delta receptors, which are increased following steroid withdrawal. As predicted by the Jones-Westbrook model, this change was accompanied by reduced receptor desensitization as well as an acceleration of the rate of recovery from rapid desensitization. A theoretical analysis of the data suggested that steroid treatment leads to receptors with a greater stability of the bound, activatable state. This was achieved by altering multiple parameters, including desensitization and gating rates, within the model. These results suggest that fluctuations in endogenous steroids result in altered GABAR kinetics which may regulate neuronal excitability.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.