ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
The human immunodeficiency virus-1 protein Tat and its discrete fragments evoke selective release of acetylcholine from human and rat cerebrocortical terminals through species-specific mechanisms.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- HIV-1 Tat-driven Glutamate Dysregulation: Implications for Cognitive Impairment in HAND.Current HIV/AIDS reports · 2026Review
- The Impact of Neurotransmitters on the Neurobiology of Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- A new perspective on HIV: effects of HIV on brain-heart axis.Frontiers in cardiovascular medicine · 2023Review
- Presynaptic Release-regulating Metabotropic Glutamate Receptors: An Update.Current neuropharmacology · 2020Review
- HIV-1 Tat: Role in Bystander Toxicity.Frontiers in cellular and infection microbiology · 2020Review
- Cognitive Burden of Common Non-antiretroviral Medications in HIV-Infected Women.Journal of acquired immune deficiency syndromes (1999) · 2018Article
- The Cholinergic Anti-Inflammatory Response and the Role of Macrophages in HIV-Induced Inflammation.International journal of molecular sciences · 2018Review
- Presynaptic mGlu1 Receptors Control GABAFrontiers in molecular neuroscience · 2018Article
- HIV, Tat and dopamine transmission.Neurobiology of disease · 2017Review
- An Overview of Human Immunodeficiency Virus Type 1-Associated Common Neurological Complications: Does Aging Pose a Challenge?Journal of Alzheimer's disease : JAD · 2017Review
- Inhibition of GABAergic Neurotransmission by HIV-1 Tat and Opioid Treatment in the Striatum Involves μ-Opioid Receptors.Frontiers in neuroscience · 2016Article
- HIV-1 Tat-Mediated Calcium Dysregulation and Neuronal Dysfunction in Vulnerable Brain Regions.Current drug targets · 2016Review
- Presynaptic Release-Regulating mGlu1 Receptors in Central Nervous System.Frontiers in pharmacology · 2016Review
- Presynaptic c-Jun N-terminal Kinase 2 regulates NMDA receptor-dependent glutamate release.Scientific reports · 2015Article
- HIV-1-Tat excites cardiac parasympathetic neurons of nucleus ambiguus and triggers prolonged bradycardia in conscious rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Roles and functions of HIV-1 Tat protein in the CNS: an overview.Virology journal · 2013Review
- Article
- Influence of integrin-blocking peptide on gadolinium- and hypertonic shrinking-induced neurotransmitter release in rat brain synaptosomes.Neurochemical research · 2008Article
- Excitatory effects of human immunodeficiency virus 1 Tat on cultured rat cerebral cortical neurons.Neuroscience · 2008Article
- Functional interactions between presynaptic NMDA receptors and metabotropic glutamate receptors co-expressed on rat and human noradrenergic terminals.British journal of pharmacology · 2007Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effect of the human immunodeficiency virus-1 protein Tat was investigated on neurotransmitter release from human and rat cortical nerve endings. Tat failed to affect the release of several neurotransmitters, such as glutamate, GABA, norepinephrine, and others, but it evoked the release of [3H]ACh via increase of cytosolic [Ca2+]. In human nerve terminals, the Tat effect partly depends on Ca2+ entry through voltage-sensitive Ca2+ channels, because Cd2+ halved the Tat-evoked release. Activation of group I metabotropic glutamate receptors (mGluR) and mobilization of Ca2+ from IP3-sensitive intraterminal stores are also involved, because the Tat effect was prevented by mGluR antagonists 2-methyl-6-(phenylethynyl)pyridine hydrochloride and 7-(hydroxyimino)cyclopropa[b]chromen-1a-carboxylate ethyl ester and by the IP3 receptor antagonists heparin and xestospongin C. Furthermore, the group I selective mGlu agonist (RS)-3,5-dihydroxyphenylglycine enhanced [3H]ACh release. In rat nerve terminals, the Tat-evoked release neither depends on external Ca2+ ions entry nor on IP3-mediated mechanisms. Tat seems to cause mobilization of Ca2+ from ryanodine-sensitive internal stores because its effect was prevented by both 8-bromo-cyclic adenosine diphosphate-ribose and dantrolene. The Tat-evoked release from human synaptosomes was mimicked by the peptide sequences Tat 32-62, Tat 49-86, and Tat 41-60. In contrast, the Tat 49-86 and Tat 61-80 fragments, but not the Tat 32-62 fragment, were active in rat synaptosomes. In conclusion, Tat elicits Ca2+-dependent [3H]ACh release by species-specific intraterminal mechanisms by binding via discrete amino acid sequences to different receptive sites on human and rat cholinergic terminals.
Indexed as
Identifiers
12890775PMC6740728W2141101470What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.