ArticleThe international journal of neuropsychopharmacology2023
Ventral Hippocampal Input to Infralimbic Cortex Is Necessary for the Therapeutic-Like Effects of Extinction in Stressed Rats.
Article in The international journal of neuropsychopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 5 citations in OpenAlex.
- A novel finding on sex-dependent diverse behavioral responses to the anticipation of a threat in a rat model of fear conditioning with the involvement of brain-derived neurotrophic factor (BDNF) in the prefrontal cortex.Learning & behavior · 2026Article
- Sex-dependent role of the ventral hippocampus, but not its projection to the medial prefrontal cortex, in a novel operant conflict-driven ethanol choice task.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- Antidepressant-like effects of extinction learning as an animal model of behavioral therapy.Molecular psychiatry · 2026Article
- Therapeutic effects of extinction require hippocampal input and BDNF signaling in IL.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Effects of chronic stress on cognitive function - From neurobiology to intervention.Neurobiology of stress · 2024Review
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2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundPosttraumatic stress disorder is characterized by deficits in cognitive flexibility related to dysfunction of the medial prefrontal cortex (mPFC). Exposure therapy can effectively reverse these deficits. Fear extinction in rodents bears similarity to exposure therapy. Extinction reverses chronic stress-induced deficits in cognitive flexibility on the attentional set-shifting test (AST), an mPFC-mediated process. This therapeutic effect requires activity of pyramidal neurons and brain derived neurotrophic factor (BDNF) signaling in infralimbic cortex (IL). However, the circuit mechanisms governing BDNF-mediated plasticity initiated by extinction in IL are unknown. The ventral hippocampus (vHipp) plays a role in regulating IL activity during extinction, and plasticity in vHipp is necessary for extinction memory consolidation. Therefore, we investigated the role of vHipp input to IL in the effects of extinction in reversing stress-induced cognitive deficits.
methodsvHipp input to IL was silenced using a Gi-Designer Receptors Exclusively Activated by Designer Drugs (DREADD) via local infusion of clozapine-N-oxide (CNO) into IL before extinction. A day later, rats were tested on AST. In a separate experiment, we tested whether vHipp input to the IL induces BDNF signaling to exert therapeutic effects. We activated the vHipp using a Gq-DREADD, and injected an anti-BDNF neutralizing antibody into IL. Rats were tested on the AST 24 hours later.
resultsSilencing the vHipp input to IL prevented the beneficial effects of extinction in reversing stress-induced cognitive deficits. Activating vHipp input to IL in the absence of extinction was sufficient to reverse stress-induced deficits in set-shifting. The beneficial effects were blocked by local infusion of a neutralizing anti-BDNF antibody into IL.
conclusionsvHipp-driven BDNF signaling in IL is critical for extinction to counteract the deleterious cognitive effects of chronic stress.
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