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Endocannabinoid Hydrolysis Generates Brain Prostaglandins That Promote Neuroinflammation
A new tissue-specific pathway for the synthesis of proinflammatory prostaglandins is described. Phospholipase A2(PLA2) enzymes are considered the primary source of arachidonic acid for cyclooxygenaseExpand
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HIV‐1 Tat and morphine have interactive effects on oligodendrocyte survival and morphology
Human immunodeficiency virus (HIV)‐infected individuals who abuse opiates show faster progression to AIDS, and enhanced incidence of HIV‐1 encephalitis. Most opiates with abuse liability areExpand
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Effects of chronic HIV-1 Tat exposure in the CNS: heightened vulnerability of males versus females to changes in cell numbers, synaptic integrity, and behavior
HIV-associated damage to the central nervous system results in cognitive and motor deficits. Anti-retroviral therapies reduce the severity of symptoms, yet the proportion of patients affected hasExpand
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Oligodendrocytes Are Targets of HIV-1 Tat: NMDA and AMPA Receptor-Mediated Effects on Survival and Development
Myelin pallor in HIV+ individuals can occur very early during the disease process. While myelin damage might partly originate from HIV-induced vascular changes, the timing suggests that myelin and/orExpand
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5α-reduced progestogens ameliorate mood-related behavioral pathology, neurotoxicity, and microgliosis associated with exposure to HIV-1 Tat
Human immunodeficiency virus (HIV) is associated with motor and mood disorders, likely influenced by reactive microgliosis and subsequent neural damage. We have recapitulated aspects of thisExpand
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Central HIV-1 Tat exposure elevates anxiety and fear conditioned responses of male mice concurrent with altered mu-opioid receptor-mediated G-protein activation and β-arrestin 2 activity in the
Co-exposure to opiates and HIV/HIV proteins results in enhanced CNS morphological and behavioral deficits in HIV(+) individuals and in animal models. Opiates with abuse liability, such as heroin andExpand
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Ibudilast attenuates expression of behavioral sensitization to cocaine in male and female rats
There are no FDA-approved pharmacotherapies for cocaine use disorder, indicating a need to identify novel reagents with therapeutic potential. Ibudilast is an anti-inflammatory glial attenuator andExpand
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HIV‐1 alters neural and glial progenitor cell dynamics in the central nervous system: Coordinated response to opiates during maturation
HIV‐associated neurocognitive disorders (HANDs) are common sequelae of human immunodeficiency virus (HIV) infection, even when viral titers are well controlled by antiretroviral therapy. Evidence inExpand
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A central role for glial CCR5 in directing the neuropathological interactions of HIV-1 Tat and opiates
BackgroundThe collective cognitive and motor deficits known as HIV-associated neurocognitive disorders (HAND) remain high even among HIV+ individuals whose antiretroviral therapy is optimized. HANDExpand
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Chronic HIV-1 Tat and HIV reduce Rbfox3/NeuN: evidence for sex-related effects.
The NeuN antibody has been widely used to identify and quantify neurons in normal and disease situations based on binding to a nuclear epitope in most types of neurons. This epitope was recentlyExpand
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