Neurotherapeutics, Journal Year: 2024, Volume and Issue: 21(4), P. e00377 - e00377
Published: May 22, 2024
Language: Английский
Neuropharmacology, Journal Year: 2022, Volume and Issue: 224, P. 109335 - 109335
Published: Nov. 17, 2022
Language: Английский
Citations
28
Translational Psychiatry, Journal Year: 2023, Volume and Issue: 13(1)
Published: July 25, 2023
Relapse is common in remitted patients with major depressive disorder (MDD). Arketamine, an (R)-enantiomer of ketamine, has persistent prophylactic actions inflammatory model depression. However, the precise mechanisms underlying these remain unknown. Given role brain-spleen axis depression, we sought to identify splenic molecular targets that play a arketamine. Lipopolysaccharide (LPS) (1.0 mg/kg) was administered 6 days after single injection arketamine (10 or saline. RNA-sequencing analysis found altered expression heme biosynthesis II pathway. Quantitative RT-PCR revealed pretreatment blocked increased genes involved pathway LPS-treated mice, namely, 5-aminolevulinase synthase 2 (Alas2), ferrochelatase (Fech), hydroxymethylbilane (Hmbs). Interestingly, there were positive correlations between and spleen weight plasma levels pro-inflammatory cytokines. We also higher ALAS2 FECH from MDD patients. Pretreatment key intermediate precursor heme, 5-aminolaevulinic acid (300 mg/kg/day for 3 days), caused splenomegaly, cytokines, depression-like behavior low-dose LPS (0.1 mg/kg)-treated mice. inhibitor, succinyl acetone (120 had effects These data suggest novel inflammation-related Therefore, could be new target prevention relapse
Language: Английский
Citations
14
Pharmacological Research, Journal Year: 2024, Volume and Issue: 200, P. 107081 - 107081
Published: Jan. 25, 2024
Ketamine, a non-competitive N-methyl-D-aspartate receptor (NMDAR) antagonist, has received much attention for its rapid antidepressant effects. A single administration of ketamine elicits and sustained effects in both humans animals. Current efforts are focused on uncovering molecular mechanisms responsible ketamine's activity. Ketamine primarily acts via the glutamatergic pathway, increasing evidence suggests that induces synaptic structural plasticity through increased translation release neurotrophic factors, activation mammalian target rapamycin (mTOR), α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPAR)-mediated potentiation. However, initial events triggering intracellular signaling cascades remain poorly understood. Over last few years, it become apparent addition to fast actions ligand-gated AMPARs NMDARs, metabotropic glutamate receptors (mGluRs), particularly mGluR5, may also play role action ketamine. Although research mGluR5 relation beneficial is still infancy, careful evaluation existing literature can identify converging trends provide new interpretations. Here, we review current regulation response from perspective propose possible mechanism linking NMDAR inhibition modulation.
Language: Английский
Citations
5
Pharmacology Biochemistry and Behavior, Journal Year: 2024, Volume and Issue: 238, P. 173736 - 173736
Published: Feb. 23, 2024
Language: Английский
Citations
5
Molecular Psychiatry, Journal Year: 2023, Volume and Issue: 28(12), P. 4977 - 4994
Published: June 30, 2023
Language: Английский
Citations
12
Pharmacology Biochemistry and Behavior, Journal Year: 2023, Volume and Issue: 233, P. 173659 - 173659
Published: Oct. 14, 2023
Language: Английский
Citations
12
Cells, Journal Year: 2024, Volume and Issue: 13(10), P. 880 - 880
Published: May 20, 2024
MicroRNAs can interfere with protein function by suppressing their messenger RNA translation or the synthesis of its related factors. The brain-derived neurotrophic factor (BDNF) is essential to proper formation and nervous system seen be regulated many microRNAs. However, understanding how microRNAs influence BDNF actions within cells requires a wider comprehension integrative regulatory mechanisms.
Language: Английский
Citations
4
Psychopharmacology, Journal Year: 2025, Volume and Issue: unknown
Published: March 17, 2025
Abstract Rationale Existing studies predominantly focus on the molecular and neurobiological mechanisms underlying Ketamine’s acute treatment effects post-traumatic stress disorder (PTSD). This emphasis has largely overlooked its sustained therapeutic effects, which hold significant potential for development of targeted interventions. Objectives systematic review examines pharmacokinetic pharmacodynamic ketamine PTSD, differentiating between immediate effects. Method A comprehensive search across databases (Web Science, Scopus, Global Health, PubMed) grey literature yielded 317 articles, where 29 met inclusion criteria. These included preclinical models clinical trials, through neurotransmitter regulation, gene expression, synaptic plasticity, neural pathways (PROSPERO ID: CRD42024582874). Results We found accumulating evidence that ketamine, involve changes in GABA, glutamate, glutamine levels, trigger re-regulation BDNF, enhancing plasticity via such as TrkB PSD-95. Other influences also include c-Fos, GSK-3, HDAC, HCN1, modulation hormones like CHR ACTH, alongside immune responses (IL-6, IL-1β, TNF-α). Sustained arise from remodulations prolonged expression. mTOR-mediated BDNF alterations GSK-3β, FkBP5, GFAP, ERK phosphorylation, epigenetic modifications (DNMT3, MeCP2, H3K27me3, mir-132, mir-206, HDAC). Conclusion promote long-term stability key brain regions, contributing to benefits. Understanding behind ketamine’s is critical developing safe effective personalised treatments, potentially leading more recovery.
Language: Английский
Citations
0
Biological Psychiatry, Journal Year: 2025, Volume and Issue: unknown
Published: March 1, 2025
Language: Английский
Citations
0
Neuropharmacology, Journal Year: 2022, Volume and Issue: 223, P. 109351 - 109351
Published: Nov. 21, 2022
Language: Английский
Citations
12