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Discover Supplement-Drug Interactions
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Last Updated: 3 years ago
supplement:
Cocaine
drug:
Cycloserine
Research Papers that Mention the Interaction
“Here, for the first time we demonstrate that cocaine induces over expression of DC-SIGN and significantly enhances virus transfer from DCs to T-cells by increasing the binding and internalization of HIV-1 in DCs.”
Cocaine Enhances DC to T-cell HIV-1 Transmission by Activating DC-SIGN/LARG/LSP1 Complex and Facilitating Infectious Synapse Formation“The present study adds to this literature by demonstrating that DCS may prevent extinction to cocaine cues in temporal and occipital brain regions.”
“Although D-cycloserine (30 mg/kg) abolished cocaine (10 mg/kg)-induced CPP, sarcosine (300 and 600 mg/kg) and D-serine (600 mg/kg) diminished the expression of such a cocaine memory.”
D-cycloserine, sarcosine and D-serine diminish the expression of cocaine-induced conditioned place preference“We previously reported that the NMDA receptor partial agonist d-cycloserine administered after pavlovian extinction of cocaine cues in the nucleus accumbens core (NAc) reduced cue-induced renewal.”
“More specifically, we demonstrate that 30 mg/kg DCS was effective at significantly accelerating the extinction of cocaine self‐administration behavior in rats.”
“We showed that 30 mg/kg DCS , but not 15 mg/kg significantly accelerated extinction of cocaine self‐administration behavior when compared with saline by almost half (4 days vs. 9 days).”
“BACKGROUND D-cycloserine DCS ), a partial N-methyl-D-aspartate receptor agonist, has been shown to enhance the extinction of both cocaine and amphetamine-induced conditioned place preference (CPP).”
“In addition, we found that cocaine significantly altered the integrity of the RNA-induced silencing complex (RISC) in HIV-1 infected macrophages and DCs compared to untreated HIV-1 infected cells.”
“We found that cocaine significantly augmented the release of EVs from uninfected and HIV-1 infected T-cells, DCs and macrophages.”
Cocaine augments neuro-inflammation via modulating extracellular vesicle release in HIV-1 infected immune cells
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