Methamphetamine-induced expression of interleukin-1β mRNA in the rat hypothalamus

Yamaguchi, Takashi; Kuraishi, Yasushi; Minami, Masabumi; Nakai, Satoru; Hirai, Yoshikatsu; Satoh, Masamichi

doi:10.1016/0304-3940(91)90766-m

Cited by 62 publications

(41 citation statements)

References 15 publications

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“…We also reported the induction of IL-1β mRNA expression in the hypothalamus by chemical nociceptive stimulus caused by an intraplanter injection of formalin (63) as well as the induction by neuronal stimulants (64,65) and immobilization stress (66). These findings suggest that brain IL-1 production is induced by noxious stimuli and plays a role in pain modulation.…”

Section: Il-1β In Pain Modulationmentioning

confidence: 80%

Brain Cytokines and Chemokines: Roles in Ischemic Injury and Pain

2006

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Abstract. Cytokines and chemokines were originally identified as essential mediators for inflammatory and immune responses. Enhanced production and release of cytokines / chemokines are observed also in the central nervous system (CNS) under diverse pathological conditions. There is growing evidence showing that brain cytokines / chemokines play crucial roles in the neuro-glio-vascular interaction underlying the pathology of various brain disorders and therefore are potential targets for development of novel and effective therapeutics for CNS diseases. Here the evidence of the involvement of cytokines / chemokines in ischemic brain injury and pain is reviewed.

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Section: Il-1β In Pain Modulationmentioning

confidence: 80%

Brain Cytokines and Chemokines: Roles in Ischemic Injury and Pain

2006

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“…IL-1b, IL-6, and NO • radicals, vice versa. Indeed, METH induced expression of IL-1b mRNA in the rat brain [31]. Cadet and his colleagues reported that METH-induced neurotoxicity and gliosis were attenuated in IL-6 knockout mice [15] and that METH injection increased the expression of transcription factor NF-AT, which promotes IL-4 expression [32], suggesting involvement of inflammatory cytokines in METHinduced neurotoxic cascade.…”

Section: Discussionmentioning

confidence: 97%

Reduction of Nuclear Peroxisome Proliferator-Activated Receptor γ Expression in Methamphetamine-Induced Neurotoxicity and Neuroprotective Effects of Ibuprofen

et al. 2008

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We examined changes in nuclear peroxisome proliferator-activated receptor gamma (PPAR gamma) in the striatum in methamphetamine (METH)-induced dopaminergic neurotoxicity, and also examined effects of treatment with drugs possessing PPAR gamma agonistic properties. The marked reduction of nuclear PPAR gamma-expressed cells was seen in the striatum 3 days after METH injections (4 mg/kg x 4, i.p. with 2-h interval). The reduction of dopamine transporter (DAT)-positive signals and PPAR gamma expression, and accumulation of activated microglial cells were significantly and dose-dependently attenuated by four injections of a nonsteroidal anti-inflammatory drug and a PPAR gamma ligand, ibuprofen (10 or 20 mg/kg x 4, s.c.) given 30 min prior to each METH injection, but not by either a low or high dose of aspirin. Either treatment of ibuprofen or aspirin, that showed no effects on METH-induced hyperthermia, significantly blocked the METH-induced striatal cyclooxygenase (COX) expression. Furthermore, the treatment of an intrinsic PPAR gamma ligand 15d-PG J2 also attenuated METH injections-induced reduction of striatal DAT. Therefore, the present study suggests the involvement of reduction of PPAR gamma expression in METH-induced neurotoxicity. Taken together with the previous report showing protective effects of other PPAR gamma ligand, these results imply that the protective effects of ibuprofen against METH-induced neurotoxicity may be based, in part, on its anti-inflammatory PPAR gamma agonistic properties, but not on its COX-inhibiting property or hypothermic effect.

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“…Several studies have reported increased expression of IL-1␤ in response to brain insults, including peripheral kainic acid (35), methamphetamine (36), intracerebral administration of Nmethyl-D-aspartate (NMDA) agonists (37,38), physical injury (39), and cerebral ischemia (40)(41)(42). Microglia are the major early source of IL-1␤ in response to kainic acid, NMDA agonists (30,35,38,43), or cerebral ischemia (42), although delayed expression has been reported by astrocytes (38,42).…”

Section: Discussionmentioning

confidence: 99%

“…It is probable that the increased levels of IL-1␤ (mRNA and protein) observed in the present study would show similar patterns of cellular expression. Interestingly, peripheral administration of methamphetamine in the rat induces a specific increase in IL-1␤ mRNA in the hypothalamus (36), but the relevance of this to neuronal injury was not considered. Likewise, audiogenic seizures have been demonstrated to increase IL-1␣ mRNA specifically in the hypothalamus and not in other regions such as the hippocampus or cortex (44).…”

Section: Discussionmentioning

confidence: 99%

Cortical cell death induced by IL-1 is mediated via actions in the hypothalamus of the rat

Allan

Parker

Collins

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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The cytokine IL-1 mediates diverse forms of neurodegeneration, but its mechanism of action is unknown. We have demonstrated previously that exogenous and endogenous IL-1 acts specifically in the rat striatum to dramatically enhance ischemic and excitotoxic brain damage and cause extensive cortical injury. Here we tested the hypothesis that this distant effect of IL-1 is mediated through polysynaptic striatal outputs to the cortex via the hypothalamus. We show that IL-1␤ injected into the rat striatum with the excitotoxin ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (S-AMPA) caused increased expression of IL-1␤ (mRNA and protein) mainly in the cortex where maximum injury occurs. Marked increases in IL-1␤ mRNA and protein were also observed in the hypothalamus. S-AMPA, injected alone into the striatum, caused only localized damage, but administration of IL-1␤ into either the striatum or the lateral hypothalamus immediately after striatal S-AMPA resulted in widespread cell loss throughout the ipsilateral cortex. Finally we showed that the cortical cell death produced by striatal coinjection of S-AMPA and IL-1␤ was significantly reduced by administration of the IL-1 receptor antagonist into the lateral hypothalamus. These data suggest that IL-1␤ can act in the hypothalamus to modify cell viability in the cortex. We conclude that IL-1-dependent pathways project from the striatum to the cortex via the hypothalamus and lead to cortical injury, and that these may contribute to a number of human neurological conditions including stroke and head trauma. E xcessive activation of glutamate receptors (excitotoxicity) contributes to a number of neurodegenerative disorders (1). Thus direct injection of glutamatergic agonists into the brains of experimental animals has proved a useful model to study, in vivo, the underlying mechanisms of cell death in such acute conditions. There is increasing interest in the role of inflammatory mediators such as IL-1 in cell death in this and other forms of neurodegeneration, such as cerebral ischemia (2).The cytokine IL-1 has diverse actions in the brain and mediates acute experimental neurodegeneration (3). Injection or overexpression of IL-1 receptor antagonist (IL-1ra) significantly inhibits neuronal damage induced in rodents by focal cerebral ischemia, traumatic brain injury, or excitotoxin administration (see ref.2). Administration of exogenous IL-1␤ fails to cause neuronal death in normal rat brain but markedly exacerbates ischemic, traumatic, or excitotoxic brain injury (4-6). When IL-1␤ is coinjected with ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (S-AMPA) in the rat striatum, extensive cell death occurs throughout the ipsilateral cortex, which is not observed after S-AMPA alone (6). The mechanism of this potent effect of IL-1␤ is not known, although in focal cerebral ischemia, exacerbation by IL-1␤ and neuroprotective actions of IL-1ra are also mediated through actions in the striatum that influence cortical damage (7). Because excitotoxicity contributes to many forms of n...

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Methamphetamine-induced expression of interleukin-1β mRNA in the rat hypothalamus

Cited by 62 publications

References 15 publications

Brain Cytokines and Chemokines: Roles in Ischemic Injury and Pain

Brain Cytokines and Chemokines: Roles in Ischemic Injury and Pain

Reduction of Nuclear Peroxisome Proliferator-Activated Receptor γ Expression in Methamphetamine-Induced Neurotoxicity and Neuroprotective Effects of Ibuprofen

Cortical cell death induced by IL-1 is mediated via actions in the hypothalamus of the rat

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