Fluoxetine attenuates stress-induced depressive-like behavior through modulation of hippocampal GAP43 and neurogenesis in male rats

Zavvari, Fahime; Nahavandi, Arezo; Goudarzi, Mina

doi:10.1016/j.jchemneu.2019.101711

Cited by 28 publications

(9 citation statements)

References 63 publications

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“…Lactate, the end-product of astrocytic glycolysis, can be transferred to neurons (Magistretti and Allaman, 2018) to support synaptic plasticity (Murphy-Royal et al, 2020). In our study, fluoxetine treatment increased PFC astrocytic lactate release in vivo and in vitro, modulating astrocytic glycolysis in corticosterone-induced depression, which may be one possible reason that fluoxetine could improve neuronal plasticity (Zavvari et al, 2020). Then, we explored how fluoxetine regulated astrocytic glycolysis in corticosterone-induced depressive state.…”

Section: Discussionmentioning

confidence: 76%

Fluoxetine increases astrocytic glucose uptake and glycolysis in corticosterone-induced depression through restricting GR-TXNIP-GLUT1 Pathway

et al. 2022

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Antidepressant fluoxetine can affect cerebral glucose metabolism in clinic, but the underlying molecular mechanism remains poorly understood. Here, we examined the effect of fluoxetine on brain regional glucose metabolism in a rat model of depression induced by repeated corticosterone injection, and explored the molecular mechanism. Fluoxetine was found to recover the decrease of 18F-fluorodeoxyglucose (18F-FDG) signal in prefrontal cortex (PFC), and increased 2-[N-(7-Nitrobenz-2-oxa-1,3-diazol-4-yl) amino]-2-deoxy-D-glucose (2-NBDG, a fluorescent glucose analog) uptake in an astrocyte-specific manner in ex vivo cultured PFC slices from corticosterone-induced depressive rats, which were consistent with its improvement of animal depressive behaviors. Furthermore, fluoxetine restricted nuclear translocation of glucocorticoid receptor (GR) to suppress the transcription of thioredoxin interacting protein (TXNIP). Subsequently, it promoted glucose transporter 1 (GLUT1)-mediated glucose uptake and glycolysis of PFC astrocytes through suppressing TXNIP expression under corticosterone-induced depressive state. More importantly, fluoxetine could improve glucose metabolism of corticosterone-stimulated astrocytes via TXNIP-GLUT1 pathway. These results demonstrated that fluoxetine increased astrocytic glucose uptake and glycolysis in corticosterone-induced depression via restricting GR-TXNIP-GLUT1 pathway. The modulation of astrocytic glucose metabolism by fluoxetine was suggested as a novel mechanism of its antidepressant action.

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Section: Discussionmentioning

confidence: 76%

Fluoxetine increases astrocytic glucose uptake and glycolysis in corticosterone-induced depression through restricting GR-TXNIP-GLUT1 Pathway

et al. 2022

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“…So, the purpose was not to compare the medicines against their authentic samples and find their API, but use the same extraction process and GC method for different solid materials, allowing the identification of similar formulas that could indicate a common origin between the seized medicines. After the analysis, it was also noted that Fluoxetine, a Serotonin-Selective Reuptake Inhibitor used as antidepressant [9], it's being employed to falsify seized samples labeled as Sibutramine and Diethylpropion.…”

Section: Resultsmentioning

confidence: 99%

Counterfeit medicines: a pilot study for chemical profiling employing a different proposal of an usual technique

Santos

Kahmann²,

Caffarate

et al. 2020

Drug Anal. Res.

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Gas chromatography (GC) is a gold standard technique used in forensic laboratories, including for the characterization of counterfeit medicines. When coupled simultaneously to flame ionization (FID) and mass detector (MS) allow the identification and quantification of medicines and drugs employing a single method, besides permitting the application of chemometric tools for forensic intelligence purposes. Here is presented a pilot project that developed and applied a qualitative method for the analysis of counterfeit medicines comprised by amphetamine-type stimulants and antidepressants, through a simple extraction procedure followed by GC-FID/MS analysis, with application of exploratory tools by Hierarchical Cluster Analysis (HCA) and Principal Component Analysis (PCA). The main purpose was to identify similarities between the all compounds detected in the irregular medicines allowing the traceability of illicit producers with the creation of a common data base. Through the analyses it was verified that different producers of counterfeit medicines labeled as Sibutramine, added a mixture of Caffeine and Benzocaine in their formulation, respecting the same ratio of 2.2:1. HCA was able to confirm these results, showing the presence of both falsifications in the same cluster, representing the best tool to identify similar characteristics among the samples – when compared to PCA. Other interesting finding was the use of Fluoxetine as a falsification of counterfeit medicines labeled as Sibutramine and Diethylpropion. Another seized sample labeled as “Nobesio Forte”, marketed as a mix of stimulants, showed only Caffeine and Lidocaine in its formulation. The pilot project applied primarily to 45 samples of counterfeit medicines containing amphetamine-type stimulants and antidepressants, showed the capability of perform the chemical profiling of counterfeit medicines in the solid form - powder, capsules and tablets. Further analysis can be performed for different types of medicines in solid form using the developed method, allowing the construction of a single database to perform the chemical profiling of counterfeit medicines, enabling the traceability of illicit producers.

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“…In this regard, we observed a similar response with a decrease in miR-16 expression in the CUMS group and an increase after FLX treatment. Other studies indicate that the antidepressant effects of FLX appear to involve neurotransmitter synthesis and anti-inflammatory action that may promote hippocampal neuroplasticity by increasing –a protein related to neuronal plasticity in the hippocampus called GAP-43 as seen on a rat model of depression [ 145 ]– and that FLX treatment can improve the depressive behavior exhibited.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic treatment with fluoxetine using the chronic unpredictable stress model induces changes in neurotransmitters and circulating miRNAs in extracellular vesicles

Estévez-Cabrera¹,

Sánchez‐Muñoz²,

Pérez‐Sánchez³

et al. 2023

Heliyon

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Fluoxetine attenuates stress-induced depressive-like behavior through modulation of hippocampal GAP43 and neurogenesis in male rats

Cited by 28 publications

References 63 publications

Fluoxetine increases astrocytic glucose uptake and glycolysis in corticosterone-induced depression through restricting GR-TXNIP-GLUT1 Pathway

Fluoxetine increases astrocytic glucose uptake and glycolysis in corticosterone-induced depression through restricting GR-TXNIP-GLUT1 Pathway

Counterfeit medicines: a pilot study for chemical profiling employing a different proposal of an usual technique

Therapeutic treatment with fluoxetine using the chronic unpredictable stress model induces changes in neurotransmitters and circulating miRNAs in extracellular vesicles

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