Role of Tumor Necrosis Factor-α in Methamphetamine-Induced Drug Dependence and Neurotoxicity

Nakajima, Akira; Yamada, Kiyofumi; Nagai, Taku; Uchiyama, Takehisa; Miyamoto, Yukio; Mamiya, Takayoshi; He, Jue; Nitta, Atsumi; Mizuno, Makoto; Tran, Manh Hung; Seto, Aika; Yoshimura, Masako; Kitaichi, Kiyoyuki; Hasegawa, Takaaki; Saito, Kuniaki; Yamada, Yasuhiro; Seishima, Mitsuru; Sekikawa, Kenji; Kim, Hyoung Chun; Nabeshima, Toshitaka

doi:10.1523/jneurosci.4847-03.2004

Cited by 160 publications

(160 citation statements)

References 89 publications

(88 reference statements)

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“…The persistent adaptation associated with the LPS/withdrawal and cytokine/withdrawal protocols is proposed to be related to behaviors associated with negative affectFa response thought to facilitate relapse to drinking (Breese et al, 2005a, c). Consequently, the argument that cytokines are involved in the neural disruption and addictive behaviors induced by other drugs of abuse (Friedman and Eisenstein, 2004;Yamada and Nabeshima, 2004;Nakajima et al, 2004) may apply to an association of cytokines to alcohol abuse (Kiefer et al, 2002). The results of the present work would be consistent with this view.…”

Section: Figuresupporting

confidence: 83%

Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Breese

Knapp

Overstreet

et al. 2007

Neuropsychopharmacol

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Previous investigations demonstrated that repeated stresses before an ethanol exposure sensitize ethanol withdrawal-induced anxietylike behavior ('anxiety'). In addition to activating the hypothalamic-pituitary-adrenal axis, acute stress also elevates cytokines in brain. Initially, to test possible cytokine involvement in this stress/withdrawal protocol, cytokines were increased in brain with 2 weekly repeated lipopolysaccharide (LPS) administrations (1000 m/kg) (LPS/withdrawal protocol) or with twice weekly intracerebroventricular (i.c.v.) administrations of the cytokines IL-1b, CCL2 (MCP-1) or TNFa (cytokine/withdrawal protocol) before exposure and withdrawal from a 5-day cycle of chronic ethanol diet. Both protocols sensitized withdrawal-induced anxiety and confirm cytokine involvement in the sensitized anxiety response. Testing of various doses of LPS (16-1000 mg/kg) and TNFa (3-100 ng, i.c.v.) demonstrated the dose-related nature of these protocols to sensitize withdrawal-induced anxiety. The sensitized anxiety was not produced by a single 5-day ethanol diet cycle or by repeated LPS or cytokine treatments alone. Likewise, sensitized anxiety in these protocols could not be attributed to differences in ethanol ingestion. When challenged with a subsequent re-exposure to a 5-day ethanol diet cycle 16 days after completion of the LPS/withdrawal or cytokine/withdrawal protocols, an increase in withdrawal-induced anxiety was observedFan indication of induction of an underlying persistent adaptive change. Finally, just as found previously with the stress/withdrawal protocol, administration of the benzodiazepine receptor antagonist flumazenil before the LPS or TNF treatments prevented anxiety sensitization. Together, these findings indicate that increased cytokine activity induces adaptive change that supports sensitization of ethanol withdrawal-induced anxiety that may be linked to GABA A -receptor function.

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Section: Figuresupporting

confidence: 83%

Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Breese

Knapp

Overstreet

et al. 2007

Neuropsychopharmacol

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“…For example, we have previously found that the expression of tissue plasminogen activator plays a positive role in morphine-induced synaptic plasticity, 19 whereas tumor necrosis factor-a expression in NAc inhibits METH-induced dependence. 18 Piccolo expression was upregulated by repeated METH administration and partial knockdown of Piccolo expression by antisense technique led to elevated synaptic DA concentration in the NAc and two major behavioral manifestations in mice: heightened hyperlocomotor activity and rewarding effect. These findings strongly show that Piccolo overexpression elicited by METH may serve as a homeostatic mechanism that prevents behavioral sensitization by maintaining the expression and activity of the plasmalemmal DAT.…”

Section: Discussionmentioning

confidence: 99%

“…18 The mice were injected with METH (1 mg kg À1 , s.c.) daily for 5 days (day 1-5), followed by locomotor activity measurement at days 1, 3 and 5. Conditioned place-preference (CPP) test was carried out according to the methods as described before but with modification in conditioning.…”

Section: Locomotor Activity and Cpp Testmentioning

confidence: 99%

Identification of Piccolo as a regulator of behavioral plasticity and dopamine transporter internalization

et al. 2008

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Dopamine transporter (DAT) internalization is a mechanism underlying the decreased dopamine reuptake caused by addictive drugs like methamphetamine (METH). We found that Piccolo, a presynaptic scaffolding protein, was overexpressed in the nucleus accumbens (NAc) of the mice repeatedly administrated with METH. Piccolo downexpression by antisense technique augmented METH-induced behavioral sensitization, conditioned reward and synaptic dopamine accumulation in NAc. Expression of Piccolo C 2 A domain attenuated METH-induced inhibition of dopamine uptake in PC12 cells expressing human DAT. Consistent with this, it slowed down the accelerated DAT internalization induced by METH, thus maintaining the presentation of plasmalemmal DAT. In immunostaining and structural modeling Piccolo C 2 A domain displays an unusual feature of sequestering membrane phosphatidylinositol 4,5-bisphosphate, which may underlie its role in modulating DAT internalization. Together, our results indicate that Piccolo upregulation induced by METH represents a homeostatic response in the NAc to excessive dopaminergic transmission. Piccolo C 2 A domain may act as a cytoskeletal regulator for plasmalemmal DAT internalization, which may underlie its contributions in behavioral plasticity.

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“…Mice deficient in the IL-6 gene (IL-6 KO) were protected from METH-induced dopaminergic neurotoxicity (5). METH neurotoxicity in mice deficient in TNF-a (TNF-a KO) was markedly increased compared to wild type mice, suggesting that TNF-a has a neuroprotective role (39). Administration of a toxic dose of METH to mice caused marked increase in COX-2 in the striatum but not the hippocampus, suggesting that the neurotoxic damage in the striatum is associated with inflammation and oxidative stress (40).…”

Section: Mechanisms Of Neurotoxicitymentioning

confidence: 99%

Methamphetamine and MDMA (Ecstasy) Neurotoxicity: 'of Mice and Men'

Itzhak¹,

Achat-Mendes²

2004

IUBMB Life

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SummaryMethamphetamine (METH) and 3,4-meythylenedioxymethamphetamine (MDMA; 'ecstasy') are currently major drugs of abuse. One of the major concerns of amphetamines abuse is their potential neurotoxic effect on dopaminergic and serotonergic neurons. Although data from human studies are somewhat limited, compelling evidence suggests that these drugs cause neurotoxicity in rodents and primates. Recent studies in transgenic and knockout mice identified the role of dopamine transporters, nitric oxide, apoptotic proteins, and inflammatory cytokines in amphetamines neurotoxicity. Further research into the mechanisms underlying the dopaminergic and serotonergic neurotoxicity and the behavioral corollaries of these neuronal insults could facilitate our understanding of the consequences of human abuse of METH and MDMA on cognition, drug-seeking behavior, extinction and relapse. IUBMB Life, 56: 249-255, 2004

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Role of Tumor Necrosis Factor-α in Methamphetamine-Induced Drug Dependence and Neurotoxicity

Abstract: Tumor necrosis factor-␣ (TNF-␣

Cited by 160 publications

References 89 publications

Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Identification of Piccolo as a regulator of behavioral plasticity and dopamine transporter internalization

Methamphetamine and MDMA (Ecstasy) Neurotoxicity: 'of Mice and Men'

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