Price · Translational psychiatry 2021 · controlled animal experiment · n=48

Lithium augmentation of ketamine increases insulin signaling and antidepressant-like active stress coping in a rodent model of treatment-resistant depression.

Cited 22 times in the scientific literature.

Level 5 - mechanism / opinion, no new human data

Preclinical animal model without human clinical data

PubMed 34824208 · doi:10.1038/s41398-021-01716-w · record verified 2026-08-28

What was done

Male Wistar rats received adrenocorticotropic hormone (ACTH; 100 µg/day i.p. for 14 days) to model antidepressant resistance and were then treated for 2 days with ketamine (10 mg/kg; n = 12), lithium (37 mg/kg; n = 12), ketamine plus lithium (10 mg/kg + 37 mg/kg; n = 12), or vehicle saline (0.9%; n = 12). Behavioral testing included open field and forced swim tests. Prefrontal cortical (PFC) subregions (infralimbic [IL] and prelimbic [PL]) and peripheral blood were collected one hour post-stress. Western blots assessed ERK, mTOR, Akt, and GSK3β levels. Bioenergetics (OCR and ECAR) in anterior PFC tissue and plasma mTOR and insulin levels via ELISA were also analyzed.

What was found

The abstract reports directions of effect and p-values without absolute numerical values. Ketamine plus lithium significantly reduced forced swim immobility time (p < 0.05) and latency to immobility (p < 0.01). Combined treatment increased plasma mTOR (p < 0.01) and insulin (p < 0.001). In the IL PFC, ketamine plus lithium increased phosphorylated-to-total mTOR (p < 0.001) and Akt (p < 0.01) ratios while decreasing ERK; conversely, in the PL PFC, pmTOR/mTOR was reduced and pERK/ERK was elevated. Prefrontal tissue bioenergetics showed no significant alteration in response to BDNF or TNFα.

Why it matters

The findings suggest lithium augmentation may overcome ketamine nonresponsiveness in refractory depression via region-specific PFC mTOR/Akt signaling and peripheral insulin pathway modulation.

Limits

The study is restricted to an animal model in male rats, limiting generalizability to humans and precluding assessment of sex-specific effects. No numerical baseline or endpoint values are reported in the abstract.

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