ArticleNeuroreport2012
Enduring cortical alterations after a single in-vivo treatment of HIV-1 Tat.
Article in Neuroreport, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 26 citations in OpenAlex.
- Methamphetamine and neuroHIV suppress astrocytic potassium channel function in the medial prefrontal cortex via different mechanisms.Frontiers in pharmacology · 2025Article
- Hyperactivity of medial prefrontal cortex pyramidal neurons occurs in a mouse model of early-stage Alzheimer's disease withoutFrontiers in pharmacology · 2023Article
- HIV-Induced Hyperactivity of Striatal Neurons Is Associated with Dysfunction of Voltage-Gated Calcium and Potassium Channels at Middle Age.Membranes · 2022Article
- Memantine Attenuates Cocaine and neuroHIV Neurotoxicity in the Medial Prefrontal Cortex.Frontiers in pharmacology · 2022Article
- Crucial Role of Central Nervous System as a Viral Anatomical Compartment for HIV-1 Infection.Microorganisms · 2021Review
- A Novel Concept is Needed for Combating Alzheimer's Disease and NeuroHIV.Alzheimers disease & dementia · 2020Article
- Triumeq Increases Excitability of Pyramidal Neurons in the Medial Prefrontal Cortex by Facilitating Voltage-Gated CaFrontiers in pharmacology · 2020Article
- Cross-talk between microglia and neurons regulates HIV latency.PLoS pathogens · 2019Article
- Aging and HIV-1 alter the function of specific KNeuroscience letters · 2019Article
- Human immunodeficiency virus Tat impairs mitochondrial fission in neurons.Cell death discovery · 2018Article
- The Role of HIV Infection in Neurologic Injury.Brain sciences · 2017Review
- Combined chronic blockade of hyper-active L-type calcium channels and NMDA receptors ameliorates HIV-1 associated hyper-excitability of mPFC pyramidal neurons.Neurobiology of disease · 2016Article
- 5α-reduced progestogens ameliorate mood-related behavioral pathology, neurotoxicity, and microgliosis associated with exposure to HIV-1 Tat.Brain, behavior, and immunity · 2016Article
- HIV-1 Transgenic Rat Prefrontal Cortex Hyper-Excitability is Enhanced by Cocaine Self-Administration.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- HIV-1 Tat-Mediated Calcium Dysregulation and Neuronal Dysfunction in Vulnerable Brain Regions.Current drug targets · 2016Review
- HIV-1 proteins accelerate HPA axis habituation in female rats.Physiology & behavior · 2015Article
- Cocaine self-administration enhances excitatory responses of pyramidal neurons in the rat medial prefrontal cortex to human immunodeficiency virus-1 Tat.The European journal of neuroscience · 2015Article
- Cortical consequences of HIV-1 Tat exposure in rats are enhanced by chronic cocaine.Current HIV research · 2015Review
- Anxiety-like behavior of mice produced by conditional central expression of the HIV-1 regulatory protein, Tat.Psychopharmacology · 2014Article
- 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
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
HIV-1 proteins, including the transactivator of transcription (Tat), are believed to be involved in HIV-associated neurocognitive disorders by disrupting Ca²⁺ homeostasis, which leads to progressive dysregulation, damage, or death of neurons in the brain. We have found previously that bath-applied Tat abnormally increased Ca²⁺ influx through overactivated, voltage-sensitive L-type Ca²⁺ channels in pyramidal neurons within the rat medial prefrontal cortex (mPFC). However, it is unknown whether the Tat-induced Ca²⁺ dysregulation was mediated by increased activity and/or the number of the L-channels. This study tested the hypothesis that transient/early exposure to Tat in vivo promoted enduring L-channel dysregulation in the mPFC without neuron loss. Accordingly, rats were administered a single intracerebroventricular injection of recombinant Tat (80 μg/20 μl; diluted by cerebrospinal fluids to pathophysiological concentrations) or vehicle. Rats were killed 14 days after injection for immunohistochemical assessments of the mPFC, motor cortex, caudate-putamen, and nucleus accumbens. Stereological estimates for positively stained cells indicated a significant increase in the number of cells expressing the pore-forming Ca(v)1.2-α1c subunit of L-channels in the mPFC compared with other regions in Tat-treated or vehicle-treated rat brains. Optical density measurements showed a Tat-induced increase in glial fibrillary acidic protein expression, indicating astrogliosis in the cortical regions. There was no significant loss of neurons in any brain region investigated. These findings indicate that transient Tat exposure in vivo induced enduring L-channel dysregulation and astrogliosis in the mPFC without neuron loss. Such maladaptations may contribute toward dysregulated Ca²⁺ homeostasis and neuropathology in the PFC in the early stages of HIV infection.
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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.