ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2023
Pharmacogenetic activation of parvalbumin interneurons in the prefrontal cortex rescues cognitive deficits induced by adolescent MK801 administration.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Synaptic plasticity of prefrontal long-range inhibition regulates cognitive flexibility.Neuron · 2026Article
- FOXG1 Transcriptionally Orchestrates ParvalbuminNeuroscience bulletin · 2026Article
- Neurodevelopmental effects of early life stress: PFC and cognition.Neuroscience and biobehavioral reviews · 2026Review
- Prefrontal parvalbumin neurons mediate working memory in a task demand-dependent manner.Nature communications · 2026Article
- Restoration of Excitation-Inhibition Balance and Improvement of Schizophrenia-like Behavioral Deficits via Electroacupuncture.CNS neuroscience & therapeutics · 2026Article
- Prefrontal parvalbumin neurons as a target for enhancing cognition in non-pathological and 22q11.2 microdeletion syndrome mice.Molecular psychiatry · 2026Article
- Prefrontal cortex interneurons and their contributions to attention, working memory, and adaptive behavior.Progress in neurobiology · 2026Review
- GluN2A-NMDA receptor inhibition disinhibits the prefrontal cortex, reduces forced swim immobility, and impairs sensorimotor gating.Acta pharmacologica Sinica · 2026Article
- Rethinking parvalbumin: From passive marker to active modulator of hippocampal circuits.IBRO neuroscience reports · 2025Article
- Prefrontal parvalbumin interneurons mediate CRHR1-dependent early-life stress-induced cognitive deficits in adolescent male mice.Molecular psychiatry · 2025Article
- GABAergic and inflammatory changes in the frontal cortex following neonatal PCP plus isolation rearing, as a dual-hit neurodevelopmental model for schizophrenia.Molecular neurobiology · 2024Article
- Physiological features of parvalbumin-expressing GABAergic interneurons contributing to high-frequency oscillations in the cerebral cortex.Current research in neurobiology · 2024Review
- SynCAM1 deficiency in the hippocampal parvalbumin interneurons contributes to sevoflurane-induced cognitive impairment in neonatal rats.CNS neuroscience & therapeutics · 2024Article
- The role of cell adhesion molecule IgSF9b at the inhibitory synapse and psychiatric disease.Neuroscience and biobehavioral reviews · 2024Review
- Distinct ACC Neural Mechanisms Underlie Authentic and Transmitted Anxiety Induced by Maternal Separation in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The cognitive symptoms of schizophrenia (SZ) present a significant clinical burden. They are treatment resistant and are the primary predictor of functional outcomes. Although the neural mechanisms underlying these deficits remain unclear, pathological GABAergic signaling likely plays an essential role. Perturbations with parvalbumin (PV)-expressing fast-spiking (FS) interneurons in the prefrontal cortex (PFC) are consistently found in post-mortem studies of patients with SZ, as well as in animal models. Our studies have shown decreased prefrontal synaptic inhibition and PV immunostaining, along with working memory and cognitive flexibility deficits in the MK801 model. To test the hypothesized association between PV cell perturbations and impaired cognition in SZ, we activated prefrontal PV cells by using an excitatory DREADD viral vector with a PV promoter to rescue the cognitive deficits induced by adolescent MK801 administration in female rats. We found that targeted pharmacogenetic upregulation of prefrontal PV interneuron activity can restore E/I balance and improve cognition in the MK801 model. Our findings support the hypothesis that the reduced PV cell activity levels disrupt GABA transmission, resulting in the disinhibition of excitatory pyramidal cells. This disinhibition leads to an elevated prefrontal excitation/inhibition (E/I) balance that could be causal for cognitive impairments. Our study provides novel insights into the causal role of PV cells in cognitive function and has clinical implications for understanding the pathophysiology and management of SZ.
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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 Socratic graph.