Insufficiency of ventral hippocampus to medial prefrontal cortex transmission explains antidepressant non-response

Papp, Mariusz; Gruca, Piotr; Łasoń, Magdalena; Litwa, Ewa; Solecki, Wojciech; Willner, Paul

doi:10.1177/02698811211048281

Cited by 10 publications

(10 citation statements)

References 137 publications

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“…Antidepressant non-responsive Wistar-Kyoto rats were subjected to chronic mild stress, 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). They found that the synergy between VEN and vHPC-mPFC OGS supported their hypothesis (Papp et al, 2021).…”

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confidence: 74%

Translational psychopharmacology

Young

2021

J Psychopharmacol

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confidence: 74%

Translational psychopharmacology

Young

2021

J Psychopharmacol

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“…Conversely, up-regulating glutamatergic synaptic transmission in NAc could increase stress susceptibility ( 116 ). Therapeutically, the vHipp-mPFC pathway enables an antidepressant response in Wistar-Kyoto (WKY) rats ( 117 ). Optogenetic activation of vHipp-mPFC can also mimic the antidepressant-like response to ketamine.…”

Section: Optogenetic Findings In Dysfunctional Neural Circuitsmentioning

confidence: 99%

Advances in optogenetic studies of depressive-like behaviors and underlying neural circuit mechanisms

Shi

Du²,

Xia³

et al. 2022

Front. Psychiatry

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BackgroundsThe neural circuit mechanisms underlying depression remain unclear. Recently optogenetics has gradually gained recognition as a novel technique to regulate the activity of neurons with light stimulation. Scientists are now transferring their focus to the function of brain regions and neural circuits in the pathogenic progress of depression. Deciphering the circuitry mechanism of depressive-like behaviors may help us better understand the symptomatology of depression. However, few studies have summarized current progress on optogenetic researches into the neural circuit mechanisms of depressive-like behaviors.AimsThis review aimed to introduce fundamental characteristics and methodologies of optogenetics, as well as how this technique achieves specific neuronal control with spatial and temporal accuracy. We mainly summarized recent progress in neural circuit discoveries in depressive-like behaviors using optogenetics and exhibited the potential of optogenetics as a tool to investigate the mechanism and possible optimization underlying antidepressant treatment such as ketamine and deep brain stimulation.MethodsA systematic review of the literature published in English mainly from 2010 to the present in databases was performed. The selected literature is then categorized and summarized according to their neural circuits and depressive-like behaviors.ConclusionsMany important discoveries have been made utilizing optogenetics. These findings support optogenetics as a powerful and potential tool for studying depression. And our comprehension to the etiology of depression and other psychiatric disorders will also be more thorough with this rapidly developing technique in the near future.

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“…Neither chronic venlafaxine nor weekly OGS of vHPC–mPFC alone was effective in reversing the effects of CMS, but the combination of chronic venlafaxine and repeated OGS restored normal behaviour in all three tests. The effect was specific to the vHPC: OGS of dHPC–mPFC afferents restored normal behaviour in the EPM and NOR test, irrespective of concomitant venlafaxine treatment, and had no effect on sucrose intake (Papp et al, 2021).…”

Section: On the Mechanism Of Non‐response To Antidepressant Drugsmentioning

confidence: 99%

Perspectives for therapy of treatment‐resistant depression

Papp

Cubała

Święcicki

et al. 2021

British J Pharmacology

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A high proportion of depressed patients fail to respond to antidepressant drug treatment. Treatment-resistant depression (TRD) is a major challenge for the psychopharmacology of mood disorders. Only in the past decade have novel treatments, including deep brain stimulation (DBS) and ketamine, been discovered that provide rapid and sometimes prolonged relief to a high proportion of TRD sufferers. In this review, we consider the current status of TRD from four perspectives: the challenge of developing an appropriate regulatory framework for novel rapidly acting antidepressants; the efficacy of non-pharmacological somatic therapies; the development of an animal model of TRD and its use to understand the neural basis of antidepressant non-response; and the potential for rapid antidepressant action from targets (such as 5-HT 1A receptors) beyond the glutamate receptor.LINKED ARTICLES: This article is part of a themed issue on New discoveries and perspectives in mental and pain disorders. To view the other articles in this section visit

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Insufficiency of ventral hippocampus to medial prefrontal cortex transmission explains antidepressant non-response

Cited by 10 publications

References 137 publications

Translational psychopharmacology

Translational psychopharmacology

Advances in optogenetic studies of depressive-like behaviors and underlying neural circuit mechanisms

Perspectives for therapy of treatment‐resistant depression

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