The neuropathology of heroin abuse

Büttner, Andreas; Mall, Gita; Penning, R.; Weis, Serge

doi:10.1016/s0379-0738(00)00204-8

Cited by 155 publications

(116 citation statements)

References 63 publications

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“…An increase of Gfap in response to morphine in different brain regions has been reported by others: ventral tegmental area , spinal cord, and hippocampus (Song and Zhao, 2001). This enhanced expression of Gfap is also observed in the hippocampus of chronic heroin abusers (Buttner et al, 2000). An increase in Gfap is associated with astrogliosis in response to brain injury and is used as an indirect measure of neurotoxicity (review in Eng et al, 2000).…”

Section: Discussionmentioning

confidence: 94%

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Marie-Claire

Courtin

Roques

et al. 2004

Neuropsychopharmacol

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It has been previously suggested that morphine can regulate the expression and function of some proteins of the cytoskeleton. In the present study, we used real-time quantitative polymerase chain reaction to examine the effects of chronic morphine administration, in rat striatum, on 14 proteins involved in microtubule polymerization and stabilization, intracellular trafficking, and serving as markers of neuronal growth and degeneration. Chronic morphine treatment led to modulation of the mRNA level of seven of the 14 genes tested. Glial fibrillary acidic protein (Gfap) and activity-regulated cytoskeleton-associated protein (Arc) mRNA were upregulated, while growth associated protein (Gap43), clathrin heavy chain (Cltc), a-tubulin, Tau, and stathmin were downregulated. In order to determine if the regulation of an mRNA correlates with a modulation of the expression of the corresponding protein, immunoblot analyses were performed. With the exception of Gap43, the levels of Cltc, Gfap, Tau, stathmin, and a-tubulin proteins were found to be in good agreement with those from mRNA quantification. These results demonstrate that neuroadaptation to chronic morphine administration in rat striatum implies modifications of the expression pattern of several genes and proteins of the cytoskeleton and cytoskeletonassociated components.

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Section: Discussionmentioning

confidence: 94%

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Marie-Claire

Courtin

Roques

et al. 2004

Neuropsychopharmacol

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“…In particular, diffuse, reactive astrocytosis, with regressive astrocytic changes, is a common postmortem finding in the brains of both HIV-seropositive and seronegative intravenous heroin abusers (Gosztonyi et al, 1993;Oehmichen et al, 1996;Buttner et al, 2000), and the reactive astroglial changes accompanying heroin abuse may be exaggerated by concurrent HIV infection (Makrigeorgi-Butera et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Synergistic increases in intracellular Ca²⁺, and the release of MCP‐1, RANTES, and IL‐6 by astrocytes treated with opiates and HIV‐1 Tat

El‐Hage

Gurwell

Singh

et al. 2005

Glia

210

257

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Recent evidence suggests that injection drug users who abuse heroin are at increased risk for CNS complications from human immunodeficiency virus (HIV) infection. Opiate drugs may intrinsically alter the pathogenesis of HIV by directly modulating immune function and by directly modifying the CNS response to HIV. Despite this, the mechanisms by which opiates increase the neuropathogenesis of HIV are uncertain. Herein we describe the effect of morphine and the HIV-1 protein toxin Tat 1-72 on astroglial function in cultures derived from ICR mice. Astroglia maintain the blood brain barrier and influence inflammatory signaling in the CNS. Astrocytes can express μ opioid receptors, and are likely targets for abused opiates, which preferentially activate μ-opioid receptors. While Tat alone disrupts astrocyte function, when combined with morphine, Tat causes synergistic increases in [Ca 2+ ] i. . Moreover, astrocyte cultures treated with morphine and Tat showed exaggerated increases in chemokine release including monocyte chemoattractant protein-1 (MCP-1) and regulated on activation, normal T cell expressed and secreted (RANTES), as well as interleukin-6 (IL-6). Morphine-Tat interactions were prevented by the μ-opioid receptor antagonist β-funaltrexamine, or by immunoneutralizing Tat 1-72 or substituting a non-toxic, deletion mutant (Tat Δ31-61 ). Our findings suggest that opiates may increase the vulnerability of the CNS to viral entry (via recruitment of monocytes/macrophages) and ensuing HIV encephalitis by synergistically increasing MCP-1 and RANTES release by astrocytes. The results further suggest ‡ Abbreviations: alpha chemokine receptor (CXCR); beta chemokine ligand (CCL); beta chemokine receptor (CCR); β-funaltrexamine (β-FNA); calcium-induced calcium release (CICR); excitatory amino acid transporter-2 (EAAT2); granulocyte macrophage colony stimulating factor (GM-CSF); granulocyte-colony stimulating factor (G-CSF); human immunodeficiency virus (HIV); human immunodeficiency virus encephalitis (HIVE); inositol trisphosphate (IP 3 ); interferon (IFN); interleukin (IL); intracellular Ca 2+ ([Ca 2+ ] i ); monocyte chemoattractant protein (MCP); nor-binaltorphimine (nor-BNI); phosphatidylinositol 3-kinase (PI3-kinase); phospholipase C-γ (PLCγ); regulated on activation, normal T cell expressed and secreted (RANTES); soluble TNF receptor subunit (sTNFR1); stem cell factor (SCF); thrombopoietin (TPO); transactivator of transcription (Tat); tumor necrosis factor-α (TNF-α); vascular endothelial growth factor (VEGF).

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“…40 Both acute and chronic effects of heroin on the brain have been described and include neurovascular disorders, leukoencephalopathy, and atrophy. 39,41 In addition to these primary or direct effects of heroin on the brain, secondary complications have to be differentiated. These are related to added impurities (either lipophilic additives ["cutting"] or crystalline impurities), and they may also be secondary to associated diseases (such as infections or epilepsy).…”

Section: Opioids and Derivativesmentioning

confidence: 99%

Addictive Illegal Drugs: Structural Neuroimaging

Geibprasert¹,

Gallucci²,

Krings³

2009

AJNR Am J Neuroradiol

102

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SUMMARY:Illegal addictive drugs can lead to functional or structural impairment of the central nervous system. This review provides an overview of the structural imaging findings on CT, MR imaging, and conventional angiography related to chronic and acute abuse of the most commonly abused illegal drugs, including cannabis, organic solvents, and amphetamines and opioids and their respective derivatives. Pathomechanisms include excitotoxicity, which may lead to an acute or subacute leukoencephalopathy, and vascular complications, including vasoconstriction, vasculitis, or hypertension, which may lead to intracranial hemorrhage or ischemia. Because clinical findings alone are often nonspecific, and afflicted patients are unlikely to admit to the substance abuse, the neuroradiologist may play an important role in establishing the diagnosis and, thereby, initiating treatment.ABBREVIATIONS: CB ϭ cannabinoid; 5-HT ϭ serotonin (5-hydroxytryptamine); MCA ϭ middle cerebral artery; MDMA ϭ 3,4-methylenedioxymethamphetamine; MRA ϭ MR angiography; PET ϭ positron-emission tomography

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The neuropathology of heroin abuse

Cited by 155 publications

References 63 publications

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Synergistic increases in intracellular Ca²⁺, and the release of MCP‐1, RANTES, and IL‐6 by astrocytes treated with opiates and HIV‐1 Tat

Addictive Illegal Drugs: Structural Neuroimaging

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The neuropathology of heroin abuse

Cited by 155 publications

References 63 publications

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Cytoskeletal Genes Regulation by Chronic Morphine Treatment in Rat Striatum

Synergistic increases in intracellular Ca2+, and the release of MCP‐1, RANTES, and IL‐6 by astrocytes treated with opiates and HIV‐1 Tat

Addictive Illegal Drugs: Structural Neuroimaging

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Product

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Synergistic increases in intracellular Ca²⁺, and the release of MCP‐1, RANTES, and IL‐6 by astrocytes treated with opiates and HIV‐1 Tat