ArticleJournal of neuroendocrinology2020
Glucocorticoid and β-adrenergic regulation of hippocampal dendritic spines.
Article in Journal of neuroendocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Impact of Particulate Matter 2.5 on Neurological Diseases: Insights Into Pathophysiological and Molecular Mechanisms.Journal of toxicology · 2025Review
- Overnight neuronal plasticity and adaptation to emotional distress.Nature reviews. Neuroscience · 2024Review
- Intense training prevents the amnestic effect of inactivation of dorsomedial striatum and induces high resistance to extinction.PloS one · 2024Article
- The Neuroendocrine Impact of Acute Stress on Synaptic Plasticity.Endocrinology · 2023Review
- Knowledge mapping of the relationship between norepinephrine and memory: a bibliometric analysis.Frontiers in endocrinology · 2023Article
- An emerging role for microglia in stress-effects on memory.The European journal of neuroscience · 2022Review
- Glucocorticoid and β-adrenergic regulation of hippocampal dendritic spines.Journal of neuroendocrinology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucocorticoid hormones are particularly potent with respect to enhancing memory formation. Notably, this occurs in close synergy with arousal (i.e., when norepinephrine levels are enhanced). In the present study, we examined whether glucocorticoid and norepinephrine hormones regulate the number of spines in hippocampal primary neurons. We report that brief administration of corticosterone or the β-adrenergic receptor agonist isoproterenol alone increases spine number. This effect becomes particularly prominent when corticosterone and isoproterenol are administered together. In parallel, corticosterone and isoproterenol alone increased the amplitude of miniature excitatory postsynaptic currents, an effect that is not amplified when both hormones are administered together. The effects of co-application of corticosterone and isoproterenol on spines could be prevented by blocking the glucocorticoid receptor antagonist RU486. Taken together, both corticosterone and β-adrenergic receptor activation increase spine number, and they exert additive effects on spine number for which activation of glucocorticoid receptors is permissive.
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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.