ArticleIBRO neuroscience reports2026
Effects of MC-100093, GLT-1 enhancer, in mesolimbic brain regions of C57BL/6 mouse exposed to hydrocodone high-dose challenge using comprehensive laboratory monitoring system.
Article in IBRO neuroscience reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Chronic exposure and overdose of opioid cause neurotoxicity through alterations of several neurotransmitters, including glutamate. Upregulating glutamate transporter 1 (GLT-1) has been shown to attenuate the behavioral and neurochemical effects of chronic exposure to drugs of abuse. This study investigated the effects of GLT-1 enhancers-MC-100093 and ceftriaxone-on locomotor activity, respiratory exchange, and glutamate transporters (GLT-1, cystine/glutamate transporter, xCT), brain derived neurotrophic factor (BDNF), and neuroinflammatory biomarkers (TNF-α and HMGB1) in nucleus accumbens (NAc) and amygdala (AMY) of C57BL/6 mice exposed to escalated doses of hydrocodone involving high dose. Male C57BL/6 mice were intraperitoneally (i.p.) injected with hydrocodone (20 mg/kg, i.p.) every other day for 13 days and then received a higher dose of hydrocodone (40 mg /kg, i.p.) on day 15. Control group received i.p. injection of saline every other day, and mice in treatment groups received MC-100093 (50 mg/kg, i.p.) or ceftriaxone (200 mg/kg, i.p.) during the last five days. This study used comprehensive laboratory animal monitoring system (CLAMS) to measure mice's respiratory frequency, locomotor activity, oxygen consumption (VO₂), and carbon dioxide production (VCO₂). The high-dose hydrocodone challenge significantly increased VO₂ and VCO₂ while reducing the respiratory exchange ratio (RER). MC-100093 and ceftriaxone attenuated hydrocodone-induced increases in VO₂ and VCO₂; however, restoration of RER occurred exclusively in MC-100093-treated mice. Furthermore, high-dose of hydrocodone downregulated GLT-1, xCT and BDNF expression, while upregulating TNF-
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