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Torgasheva, N.

Publications and source records attributed to Torgasheva, N..

2 recordsLinked to original sources

(S)-ketamine augments behavioral and physiological responses to Δ9-tetrahydrocannabinol

(S)-ketamine is a fast-acting therapeutic to manage treatment-resistant depression as well as psychiatric emergencies. As the non-prescribed use of ketamine has rapidly increased over the past decade, its possible interactions with other recreational drugs are of increasing interest. Here, we addressed if {Delta}9-tetrahydrocannabinol (THC), the main psychoactive constituent of Cannabis sp., and (S)-ketamine could affect each others psychoactive profile in a pharmacological triad. In healthy male mice, the sequential use of (S)-ketamine followed by THC at human-relevant doses did not result in either synergistic or antagonistic effects acutely. In contrast, THC-induced hypothermia was nearly doubled by subsequent (S)-ketamine administration. THC-induced hypolocomotion was not only prolonged by (S)-ketamine, but axial rotation and stumbling during ambulation in an open field were increased in subjects exposed sequentially to both drugs. Likewise, the performance of subjects exposed to THC and then (S)-ketamine worsened on a rotarod. Combined drug treatment led to unusual epinephrine and corticosterone profiles in blood plasma. We suggest that (S)-ketamine augments adverse THC effects, which at the endocrine level invoke the acute deregulation of the hypothalamus-pituitary-adrenal axis. Our findings support the clinical notion that combining cannabis and (S)-ketamine should be avoided.

pharmacology and toxicology↗

Edited Filamin A in myeloid cells reduces intestinal inflammation and protects from colitis

Patho-mechanistic origins and disease dynamics of ulcerative colitis are still poorly understood. The actin-crosslinker Filamin A (FLNA) impacts cellular responses through interaction with cytosolic proteins. FLNA exists in two forms that differ only in one amino acid: genome-encoded FLNAQ and FLNAR - generated by post-transcriptional A-to-I editing. FLNA is edited in fibroblasts, smooth muscle- and endothelial cells in the colon. We identified the FLNA editing status as a key determinant of colitis severity. FLNA editing was highest in healthy colons and reduced during acute murine and human colitis. Mice that exclusively express edited FLNAR and do not downregulate editing upon challenge were highly resistant to DSS-induced colitis, whereas fully unedited FLNAQ animals developed severe inflammation. While the genetic induction of FLNA editing influenced transcriptional states of structural cells and the microbiome composition, we found that FLNAR exerts protection specifically via its influence on myeloid cells, which are not edited under physiological conditions. Introducing fixed, fully edited FLNAR did not hamper normal cell migration but reduced macrophage inflammation and rendered neutrophils less prone to NETosis. In conclusion, loss of FLNA editing correlates with colitis severity, and targeted FLNA editing of myeloid cells might serve as a novel therapeutic approach in intestinal inflammation. SummaryIn this study, Gawish et al. show that RNA editing of the actin cross-linker FLNA is similarly regulated in mice and humans and that the targeted induction of edited FLNAR in myeloid cells governs resistance to DSS-induced colitis, revealing its potential in IBD therapy.

molecular biology↗