Methamphetamine induced neuroinflammation in mouse brain and microglial cell line BV2: Roles of the TLR4/TRIF/Peli1 signaling axis

Yang, Tingyu; Zang, Songsong; Wang, Yixin; Zhu, Yuanhui; Jiang, Lei; Chen, Xufeng; Zhang, Xiaobao; Cheng, Jie; Gao, Rong; Xiao, Hang; Wang, Jun

doi:10.1016/j.toxlet.2020.07.028

Cited by 27 publications

(16 citation statements)

References 31 publications

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“…Its psychoactive effects are mediated through neurotransmitter (dopamine, serotonin and norepinephrine) release [7] and blockage of intracellular vesicular monoamine transporter 2 (VMAT 2) activity [8]. Neuroinflammation [9] and neuronal cell necrosis and apoptosis, particularly in the mesolimbic regions [10], then ensues from a combination of oxidative stress from degradation of excess neurotransmitters [11], activation of innate immune responses such as the toll-like receptors [9] and DNA damage [12].…”

Section: Ma: Mechanisms Of Actionmentioning

confidence: 99%

Prenatal methamphetamine—impact on the mother and child—a review

et al. 2021

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Methamphetamine (MA) is the second most commonly used illicit drug in the world, after cannabis. There are limited data on the outcomes of pregnant MA users but there is rapidly emerging evidence to suggest that they are more vulnerable, marginalized and impoverished compared with other drug‐using mothers. MA use during pregnancy is associated with worse pregnancy outcomes and significantly higher rates of co‐existing health and psychosocial problems. Newborn infants exposed to MA are at increased risk of perinatal complications, present differently at birth to infants exposed to other drugs of dependency such as opioids and have poorer neurological adaptation and feeding difficulties. Sparse literature from neuroimaging and cohort studies suggests that the neurocognitive deficits in MA exposed children persist, even into adulthood. Current clinical practice guidelines for the care of substance exposed pregnant women are opioid‐centric with little attention paid to the consequences of prenatal MA exposure.

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Section: Ma: Mechanisms Of Actionmentioning

confidence: 99%

Prenatal methamphetamine—impact on the mother and child—a review

et al. 2021

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“…Accordingly, we aimed to characterize if PRR innate immune modulators, particularly the TLRs and RAGE may be altered, as both have been implied in microglia induced neurotoxicity and neuroinflammation in drug addiction [25,36,40,42,43,45,46,79]. Unique attention has been given to TLR4 signaling: this is seemingly associated with METH induced activation of glial cells in hippocampus [44], increased DA in the NAc shell [36], enhanced cytokine expression in the cortex [37], and reduced pro-inflammatory mediators in microglia-like cells upon LPS stimulation [38]. However, our results dismiss the assumption that either striatal RAGE or TLR2, TLR4, and TLR7 could be directly involved in the observed glial activation.…”

Section: Discussionmentioning

confidence: 99%

“…For example, METH is well-known for inducing striatal DA nerve terminal damage (e.g., long-term DA, tyrosine hydroxylase (TH) depletion, DAT inactivation, and reduction in function of vesicle monoamine transporter (VMAT)) and degeneration of fine unmyelinated axons and apoptosis [10,26,35]. Additionally, METH induced neuroinflammation has been widely reported either in vitro [36][37][38] or in vivo [35][36][37]39], seemingly mediated by glial activation [35]. Although neuroimmune modulation has been claimed responsible [25,35,40], some authors have recently stood in contrast to those claims of excessive and detrimental neuroinflammation believed to contribute and exacerbate METH neurotoxicity [41].…”

Section: Introductionmentioning

confidence: 99%

“…TLR4 signaling seems to be involved in drug reward-associated behaviors and proinflammatory responses, contributing to the development of drug addiction [36,43]. Coherently, the TLR4/NFκB signaling pathway has been recently and increasingly reported to be associated with METH induced activation of glial cells in hippocampus [44], increased DA in the NAc shell [36], enhanced cytokine expression in the cortex [37], and reduced pro-inflammatory mediators in microglia-like cells upon LPS stimulation [38]. Additionally, the receptor for advanced glycation endproducts (RAGE), described to recognize glycosylated proteins and lipids in the forms of advanced glycation endproducts (AGEs), also detecting DAMPs [42], seems to play a pivotal role in synaptic function, glial response, and inflammation homeostasis when upregulated [45].…”

Section: Introductionmentioning

confidence: 99%

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Acute MDPV Binge Paradigm on Mice Emotional Behavior and Glial Signature

et al. 2021

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3,4-Methylenedioxypyrovalerone (MDPV), a widely available synthetic cathinone, is a popular substitute for classical controlled drugs of abuse, such as methamphetamine (METH). Although MDPV poses public health risks, its neuropharmacological profile remains poorly explored. This study aimed to provide evidence on that direction. Accordingly, C57BL/6J mice were exposed to a binge MDPV or METH regimen (four intraperitoneal injections every 2 h, 10 mg/kg). Locomotor, exploratory, and emotional behavior, in addition to striatal neurotoxicity and glial signature, were assessed within 18–24 h, a known time-window encompassing classical amphetamine dopaminergic neurotoxicity. MDPV resulted in unchanged locomotor activity (open field test) and emotional behavior (elevated plus maze, splash test, tail suspension test). Additionally, striatal TH (METH neurotoxicity hallmark), Iba-1 (microglia), GFAP (astrocyte), RAGE, and TLR2/4/7 (immune modulators) protein densities remained unchanged after MDPV-exposure. Expectedly, and in sheer contrast with MDPV, METH resulted in decrease general locomotor activity paralleled by a significant striatal TH depletion, astrogliosis, and microglia arborization alterations (Sholl analysis). This comparative study newly highlights that binge MDPV-exposure comes without evident behavioral, neurochemical, and glial changes at a time-point where METH-induced striatal neurotoxicity is clearly evident. Nevertheless, neuropharmacological MDPV signature needs further profiling at different time-points, regimens, and brain regions.

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“…Although both TNF-α and IL-1β, cytokines that modulate the activity of serotonin, dopamine, and glutamate, are canonically increased during viral infections, such as HIV ( Chivero et al, 2017 ; Vartak-Sharma et al, 2014 ) and Covid-19 ( McElvaney et al, 2020 ; Zhang et al, 2020 ), substances of abuse can be both immunostimulatory and immunosuppressive. For instance, inflammatory cytokines and chemokines are increased and decreased following exposure to cocaine ( Atluri et al, 2016 ; Kovalevich et al, 2015 ; Montesinos et al, 2020 ; Souza et al, 2021 ), methamphetamine ( Karimi-Haghighi et al, 2020 ; Kays and Yamamoto, 2019 ; Wang et al, 2018 ; Yang et al, 2020b ) and/or alcohol ( Barr et al, 2016 ; Crews et al, 2006 ) and dysregulated following opioid exposure ( Cisneros and Cunningham, 2021 ; Ezeomah et al, 2020 ). For example, we demonstrated increased and decreased inflammation in the nucleus accumbens relative to the hippocampus in rats withdrawn from chronic self-administration of the opioid fentanyl; these outcomes positively correlated to expression of specific host pattern recognition receptors that trigger inflammatory cascades ( Cisneros and Cunningham, 2021 ; Ezeomah et al, 2020 ).…”

Section: Inflammation In Sudsmentioning

confidence: 99%