ArticleMolecular psychiatry2020
Emergence of 5-HT5A signaling in parvalbumin neurons mediates delayed antidepressant action.
Article in Molecular psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 52 citations in OpenAlex.
- Serotonin Modulation of Dorsoventral Hippocampus in Physiology and Schizophrenia.International journal of molecular sciences · 2025Review
- Characterization of Neurensin-2 knockout mice: insights into stress-resilience mechanisms.Translational psychiatry · 2025Article
- Activation of 5-HTPharmacological reports : PR · 2024Article
- Basolateral amygdala parvalbumin and cholecystokinin-expressing GABAergic neurons modulate depressive and anxiety-like behaviors.Translational psychiatry · 2024Article
- The involvement of KTranslational psychiatry · 2024Review
- Uncovering the unique characteristics of different groups of 5-HTPharmacological reports : PR · 2024Article
- Contribution of the Opioid System to the Antidepressant Effects of Fluoxetine.Biological psychiatry · 2022Article
- Inactive and active state structures template selective tools for the human 5-HTNature structural & molecular biology · 2022Article
- Structure-Based Design of a Chemical Probe Set for the 5-HTJournal of medicinal chemistry · 2022Article
- S100A10 and its binding partners in depression and antidepressant actions.Frontiers in molecular neuroscience · 2022Review
- Molecular and Cellular Adaptations in Hippocampal Parvalbumin Neurons Mediate Behavioral Responses to Chronic Social Stress.Frontiers in molecular neuroscience · 2022Article
- Hippocampal cAMP regulates HCN channel function on two time scales with differential effects on animal behavior.Science translational medicine · 2021Article
- Parvalbumin interneuron alterations in stress-related mood disorders: A systematic review.Neurobiology of stress · 2021Review
- Identification of Neurensin-2 as a novel modulator of emotional behavior.Molecular psychiatry · 2021Article
- Activation of the p11/SMARCA3/Neurensin-2 pathway in parvalbumin interneurons mediates the response to chronic antidepressants.Molecular psychiatry · 2021Article
- Article
- Modulation of the Serotonergic Receptosome in the Treatment of Anxiety and Depression: A Narrative Review of the Experimental Evidence.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Article
- Advances in depression research: second special issue, 2020, with highlights on biological mechanisms, clinical features, co-morbidity, genetics, imaging, and treatment.Molecular psychiatry · 2020Article
- Advances in depression research: special issue, 2020, with three research articles by Paul Greengard.Molecular psychiatry · 2020Article
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6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The behavioral response to antidepressants is closely associated with physiological changes in the function of neurons in the hippocampal dentate gyrus (DG). Parvalbumin interneurons are a major class of GABAergic neurons, essential for DG function, and are involved in the pathophysiology of several neuropsychiatric disorders. However, little is known about the role(s) of these neurons in major depressive disorder or in mediating the delayed behavioral response to antidepressants. Here we show, in mice, that hippocampal parvalbumin interneurons express functionally silent serotonin 5A receptors, which translocate to the cell membrane and become active upon chronic, but not acute, treatment with a selective serotonin reuptake inhibitor (SSRI). Activation of these serotonergic receptors in these neurons initiates a signaling cascade through which Gi-protein reduces cAMP levels and attenuates protein kinase A and protein phosphatase 2A activities. This results in increased phosphorylation and inhibition of Kv3.1β channels, and thereby reduces the firing of the parvalbumin neurons. Through the loss of this signaling pathway in these neurons, conditional deletion of the serotonin 5A receptor leads to the loss of the physiological and behavioral responses to chronic antidepressants.
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