ArticleNeuroscience2015
Exogenous progesterone exacerbates running response of adolescent female mice to repeated food restriction stress by changing α4-GABAA receptor activity of hippocampal pyramidal cells.
Article in Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.
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Who cites it
13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 22 citations in OpenAlex.
- Animal Models for Anorexia Nervosa-A Systematic Review.Frontiers in human neuroscience · 2020Pooled it
- Activity Based Anorexia as an Animal Model for Anorexia Nervosa-A Systematic Review.Frontiers in nutrition · 2019Pooled it
- Examining the biological causes of eating disorders to inform treatment strategies.Nature reviews. Neuroscience · 2025Review
- Supportive care of female hormones in brain health: what and how?Frontiers in pharmacology · 2024Review
- GABAergic interneurons' feedback inhibition of dorsal raphe-projecting pyramidal neurons of the medial prefrontal cortex suppresses feeding of adolescent female mice undergoing activity-based anorexia.Brain structure & function · 2022Article
- Voluntary Wheel Running Exercise Evoked by Food-Restriction Stress Exacerbates Weight Loss of Adolescent Female Rats But Also Promotes Resilience by Enhancing GABAergic Inhibition of Pyramidal Neurons in the Dorsal Hippocampus.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- α4βδ-GABAJournal of neuroscience research · 2018Article
- α4-GABAMolecular and cellular neurosciences · 2018Article
- Variant BDNF-Val66Met Polymorphism is Associated with Layer-Specific Alterations in GABAergic Innervation of Pyramidal Neurons, Elevated Anxiety and Reduced Vulnerability of Adolescent Male Mice to Activity-Based Anorexia.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- NR2A- and NR2B-NMDA receptors and drebrin within postsynaptic spines of the hippocampus correlate with hunger-evoked exercise.Brain structure & function · 2017Article
- Review
- THE NEUROBIOLOGICAL ROOTS OF INDIVIDUALITY AND ANXIETY.Scientia (Bristol, England) · 2016Article
- The Role of Psychotropic Medications in the Management of Anorexia Nervosa: Rationale, Evidence and Future Prospects.CNS drugs · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Adolescent females are particularly vulnerable to mental illnesses with co-morbidity of anxiety, such as anorexia nervosa (AN). We used an animal model of AN, called activity-based anorexia (ABA), to investigate the neurobiological basis of vulnerability to repeated, food restriction (FR) stress-evoked anxiety. Twenty-one of 23 adolescent female mice responded to the 1st FR with increased wheel-running activity (WRA), even during the limited period of food access, thereby capturing AN's symptoms of voluntary FR and over-exercise. Baseline WRA was an excellent predictor of FR-elicited WRA (severity of ABA, SOA), with high baseline runners responding to FR with minimal SOA (i.e., negative correlation). Nine gained resistance to ABA following the 1st FR. Even though allopregnanolone (3α-OH-5α-pregnan-20-one, THP), the metabolite of progesterone (P4), is a well-recognized anxiolytic agent, subcutaneous P4 to these ABA-resistant animals during the 2nd FR was exacerbative, evoking greater WRA than the counterpart resistant group that received oil vehicle, only. Moreover, P4 had no WRA-reducing effect on animals that remained ABA-vulnerable. To explain the sensitizing effect of P4 upon the resistant mice, we examined the relationship between P4 treatment and levels of the α4 subunit of GABAARs at spines of pyramidal cells of the hippocampal CA1, a parameter previously shown to correlate with resistance to ABA. α4 levels at spine membrane correlated strongly and negatively with SOA during the 1st ABA (prior to P4 injection), confirming previous findings. α4 levels were greater among P4-treated animals that had gained resistance than of vehicle-treated resistant animals or of the vulnerable animals with or without P4. We propose that α4-GABAARs play a protective role by counterbalancing the ABA-induced increase in excitability of CA1 pyramidal neurons, and although exogenous P4's metabolite, THP, enhances α4 expression, especially among those that can gain resistance, it also interferes with α4-GABAARs' protective role by desensitizing α4-GABAARs.
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