ArticleNeurotoxicity research2011
Differences in NMDA receptor expression during human development determine the response of neurons to HIV-tat-mediated neurotoxicity.
Article in Neurotoxicity research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
21 citing papers in PubMed, 23 citations in OpenAlex.
- A new perspective on HIV: effects of HIV on brain-heart axis.Frontiers in cardiovascular medicine · 2023Review
- HIV-Proteins-Associated CNS Neurotoxicity, Their Mediators, and Alternative Treatments.Cellular and molecular neurobiology · 2022Review
- Cerebral organoids as tools to identify the developmental roots of autism.Molecular autism · 2020Review
- The Glutamate System as a Crucial Regulator of CNS Toxicity and Survival of HIV Reservoirs.Frontiers in cellular and infection microbiology · 2020Review
- Cerebral organoids exhibit mature neurons and astrocytes and recapitulate electrophysiological activity of the human brain.Neural regeneration research · 2019Review
- The role of connexin and pannexin containing channels in the innate and acquired immune response.Biochimica et biophysica acta. Biomembranes · 2018Review
- HIV-1 Tat-Mediated Calcium Dysregulation and Neuronal Dysfunction in Vulnerable Brain Regions.Current drug targets · 2016Review
- The cross-talk of HIV-1 Tat and methamphetamine in HIV-associated neurocognitive disorders.Frontiers in microbiology · 2015Review
- Redox control of microglial function: molecular mechanisms and functional significance.Antioxidants & redox signaling · 2014Review
- Interactive HIV-1 Tat and morphine-induced synaptodendritic injury is triggered through focal disruptions in Na⁺ influx, mitochondrial instability, and Ca²⁺ overload.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Role of connexin/pannexin containing channels in infectious diseases.FEBS letters · 2014Review
- Roles and functions of HIV-1 Tat protein in the CNS: an overview.Virology journal · 2013Review
- Drug induced increases in CNS dopamine alter monocyte, macrophage and T cell functions: implications for HAND.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2013Review
- Curcumin ameliorates hippocampal neuron damage induced by human immunodeficiency virus-1.Neural regeneration research · 2013Article
- Synaptic dysfunction in the hippocampus accompanies learning and memory deficits in human immunodeficiency virus type-1 Tat transgenic mice.Biological psychiatry · 2013Article
- Differential roles for caspase-mediated and calpain-mediated cell death in 1- and 3-week-old rat cortical cultures.Neuroreport · 2012Article
- Morphine potentiates neurodegenerative effects of HIV-1 Tat through actions at μ-opioid receptor-expressing glia.Brain : a journal of neurology · 2011Article
- Article
- Human immunodeficiency virus type 1 Tat modulates proliferation and differentiation of human neural precursor cells: implication in NeuroAIDS.Journal of neurovirology · 2010Article
- Mechanisms of HIV-tat-induced phosphorylation of N-methyl-D-aspartate receptor subunit 2A in human primary neurons: implications for neuroAIDS pathogenesis.The American journal of pathology · 2010Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
HIV infection of the CNS can result in neurologic dysfunction in a significant number of infected individuals. NeuroAIDS is characterized by neuronal injury and loss, yet there is no evidence of HIV infection in neurons. Thus, neuronal damage and dropout are likely due to indirect effects of HIV infection of other CNS cells, through elaboration of inflammatory factors and neurotoxic viral proteins, including the viral transactivating protein tat. We and others demonstrated that tat induces apoptosis in differentiated mature human neurons. We now demonstrate that the high level of tat toxicity observed in human neurons involves specific developmental stages that correlate with N-methyl-D-aspartate receptor (NMDAR) expression, and that tat toxicity is also dependent upon the species being analyzed. Our results indicate that tat treatment of primary cultures of differentiated human neurons with significant amounts of NMDAR expression induces extensive apoptosis. In contrast, tat treatment induces only low levels of apoptosis in primary cultures of immature human neurons with low or minimal expression of NMDAR. In addition, tat treatment has minimal effect on rat hippocampal neurons in culture, despite their high expression of NMDAR. We propose that this difference may be due to low expression of the NR2A subunit. These findings are important for an understanding of the many differences among tissue culture systems and species used to study HIV-tat-mediated toxicity.
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Registered trials
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