ArticleJournal of psychopharmacology (Oxford, England)2021
Insufficiency of ventral hippocampus to medial prefrontal cortex transmission explains antidepressant non-response.
Article in Journal of psychopharmacology (Oxford, England), 2021. 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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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Efficacy of Venlafaxine and Deep Brain Stimulation Against the Effects of Hippocampal Lesion with Ibotenic Acid in Animals Exposed to the Chronic Mild Stress Model of Depression.Current neuropharmacology · 2026Article
- Frequency-Dependent Modulation of Short-Term Neuronal Dynamics in the Female and Male Dorsal and Ventral Rat Hippocampus.International journal of molecular sciences · 2025Article
- [Neuronal plasticity changes in the central amygdala and prelimbic cortex network in mice with chronic unpredictable mild stress-induced depression].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Increasing Adiponectin Signaling by Sub-Chronic AdipoRon Treatment Elicits Antidepressant- and Anxiolytic-Like Effects Independent of Changes in Hippocampal Plasticity.Biomedicines · 2023Article
- Advances in optogenetic studies of depressive-like behaviors and underlying neural circuit mechanisms.Frontiers in psychiatry · 2022Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThere is extensive evidence that antidepressant drugs restore normal brain function by repairing damage to ventral hippocampus (vHPC) and medial prefrontal cortex (mPFC). While the damage is more extensive in hippocampus, the evidence of treatments, such as deep brain stimulation, suggests that functional changes in prefrontal cortex may be more critical. We hypothesized that antidepressant non-response may result from an insufficiency of transmission from vHPC to mPFC.
methodAntidepressant non-responsive Wistar Kyoto (WKY) rats were subjected to chronic mild stress (CMS), then treated with chronic daily administration of the antidepressant drug venlafaxine (VEN) and/or repeated weekly optogenetic stimulation (OGS) of afferents to mPFC originating from vHPC or dorsal HPC (dHPC).
resultsAs in many previous studies, CMS decreased sucrose intake, open-arm entries on the elevated plus maze (EPM), and novel object recognition (NOR). Neither VEN nor vHPC-mPFC OGS alone was effective in reversing the effects of CMS, but the combination of chronic VEN and repeated OGS restored normal behaviour on all three measures. dHPC-mPFC OGS restored normal behaviour in the EPM and NOR test irrespective of concomitant VEN treatment, and had no effect on sucrose intake.
conclusionsThe synergism between VEN and vHPC-mPFC OGS supports the hypothesis that the antidepressant non-responsiveness of WKY rats results from a failure of antidepressant treatment fully to restore transmission in the vHPC-mPFC pathway.
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