ArticleNeurochemical research2025
Up-regulation of Oxidative Burden, NFκB, and D1 Receptor Is Involved in the Neuropsychotoxic Behaviors Induced by Camfetamine, a New Psychoactive Substance; Involvements of the Neuromodulation by GPx-1 Gene.
Article in Neurochemical research, 2025. 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
An analeptic camfetamine (CFA) is a psychostimulant with complex effects, however, its psychobehavioral characteristics are unclear. As escalating evidence suggests that psychostimulant-induced behaviors are associated with oxidative stress and dopaminergic alterations, we examined whether CFA-mediated psychobehavioral mechanism requires these alterations. Conditioned place preference (CPP) and behavioral sensitization (BS) induced by CFA (7.5 mg/kg, i.p.) were evaluated in male wild-type (WT) and glutathione peroxidase (GPx)-1 knockout (KO) mice. Redox parameters, dopamine D1/D2 receptor expression, and nuclear factor kappa B (NFκB) DNA binding activity were examined in the striatum. The D1 receptor antagonist SCH 23,390 and NFκB inhibitor pyrrolidine dithiocarbamate (PDTC) were applied to investigate the psychotoxic mechanism of CFA. CFA significantly enhanced superoxide dismutase (SOD)-1 and SOD-2 levels without compensative inductions of GPx/GPx-1 level, leading to increases in oxidative markers. CFA did not significantly affect D2 receptor expression, but significantly increased D1 receptor expression and NFκB activity. D1 receptor immunoreactivity and phospho-NFκB-immunoreactivity induced by CFA were co-localized in the same cells. These changes, along with CFA-induced CPP and BS, were more prominent in GPx-1 KO mice than those in WT mice, suggesting a protective role of GPx-1. SCH 23,390 and PDTC mitigated CPP and BS; PDTC attenuated CFA-induced D1 receptor upregulation, whereas SCH 23,390 did not affect NFκB activity, suggesting NFκB is an upstream molecule for CFA-induced D1 receptor activation. Combined results suggest that CFA-induced abnormal behaviors require oxidative stress, NFκB and D1 receptor activations. GPx/GPx-1 serves as a protective modulator against CFA-induced neuropsychotoxicity.
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