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Translational control by ketamine and its implications for comorbid cognitive deficits in depressive disorders

Vern Lewis, Brandon Rodrigue, Emma J. Arsenault, Molly Zhang, Fatimeh-Frouh Taghavi-Abkuh, W. Silva, Mysa Myers, E. Matta-Camacho, Argel Aguilar-Valles

Journal of Neurochemistry June 9, 2022 DOI: 10.1111/jnc.15652 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Intervention Ketamine
Measures forced swim test, novelty suppressed feeding test
Topics Depression Esketamine Ketamine
Key findings The authors argue that ketamine's rapid antidepressant effects depend on activation of neuronal mRNA translation through the mTORC1 effector pathways 4E-BP1/2 and eEF2K, which mediate synaptic plasticity and antidepressant-like behaviors in rodents. They contend that preclinical data implicate these translation pathways in mood symptoms of major depressive disorder, while noting it remains unclear whether ketamine's pro-cognitive effects engage the same pathways or are consistently observed in treatment-resistant patients.

Abstract

Ketamine has shown antidepressant effects in patients with major depressive disorder (MDD) resistant to first‐line treatments and approved for use in this patient population. Ketamine induces several forms of synaptic plasticity, which are proposed to underlie its antidepressant effects. However, the molecular mechanism of action directly responsible for ketamine's antidepressant effects remains under active investigation. It was recently demonstrated that the effectors of the mammalian target of rapamycin complex 1 (mTORC1) signalling pathway, namely, eukaryotic initiation factor 4E (eIF4E) binding proteins 1 and 2 (4E‐BP1 and 4E‐BP2), are central in mediating ketamine‐induced synaptic plasticity and behavioural antidepressant‐like effect. 4E‐BPs are a family of messenger ribonucleic acid (mRNA) translation repressors inactivated by mTORC1. We observed that their expression in inhibitory interneurons mediates ketamine's effects in the forced swim and novelty suppressed feeding tests and the long‐lasting inhibition of GABAergic neurotransmission in the hippocampus. In addition, another effector pathway that regulates translation elongation downstream of mTORC1, the eukaryotic elongation factor 2 kinase (eEF2K), has been implicated in ketamine's behavioural effects. We will discuss how ketamine's rapid antidepressant effect depends on the activation of neuronal mRNA translation through 4E‐BP1/2 and eEF2K. Furthermore, given that these pathways also regulate cognitive functions, we will discuss the evidence of ketamine's effect on cognitive function in MDD. Overall, the data accrued from pre‐clinical research have implicated the mRNA translation pathways in treating mood symptoms of MDD. However, it is yet unclear whether the pro‐cognitive potential of subanesthetic ketamine in rodents also engages these pathways and whether such an effect is consistently observed in the treatment‐resistant MDD population.

Comparable studies

Other narrative reviews on ketamine for depression, most cited first.

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