ArticleJournal of neurovirology2016
HIV-1 Tat causes cognitive deficits and selective loss of parvalbumin, somatostatin, and neuronal nitric oxide synthase expressing hippocampal CA1 interneuron subpopulations.
Article in Journal of neurovirology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 70 citations in OpenAlex.
- HIV-1 Tat expression drives progressive synaptic decline: evidence from longitudinal [NeuroImmune pharmacology and therapeutics · 2026Article
- Comprehensive analysis of spinal cord inflammatory factors in HIV Tat-induced neuropathy in mice.Neuroscience · 2026Article
- Neuroinflammatory and Neurodegenerative Roles of HIV-1 Tat: A Review of Recent Evidence.Advances in experimental medicine and biology · 2026Review
- Osteopontin knockdown reverses HIV-induced cognitive deficits and influences motivation-related behavior.Brain, behavior, and immunity · 2026Article
- Xenon gas as a potential treatment for opioid use disorder, alcohol use disorder, and related disorders.Medical gas research · 2025Review
- HIV-1 Tat protein alters medial prefrontal cortex neuronal activity and recognition memory.iScience · 2025Article
- SIV infection induces alterations in gene expression and loss of interneurons in Rhesus Macaque frontal cortex during early systemic infection.Translational psychiatry · 2025Article
- Sex related differences in cognitive deficits: Disrupted Arc/Arg3.1 signaling in an HIV model.Neuroscience letters · 2025Article
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- GABAergic and inflammatory changes in the frontal cortex following neonatal PCP plus isolation rearing, as a dual-hit neurodevelopmental model for schizophrenia.Molecular neurobiology · 2024Article
- Neuropathogenic role of astrocyte-derived extracellular vesicles in HIV-associated neurocognitive disorders.Journal of extracellular vesicles · 2024Article
- Effects of acute ΔBrain research · 2024Article
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- Therapeutically targeting the consequences of HIV-1-associated gastrointestinal dysbiosis: Implications for neurocognitive and affective alterations.Pharmacology, biochemistry, and behavior · 2023Article
- Progressive Degeneration and Adaptive Excitability in Dopamine D1 and D2 Receptor-Expressing Striatal Neurons Exposed to HIV-1 Tat and Morphine.Cellular and molecular neurobiology · 2023Article
- Chronic methamphetamine exposure exerts few effects on the iTat mouse model of HIV, but blocks Tat expression-induced slowed reward retrieval.Behavioural brain research · 2023Article
- Circulating endothelial and angiogenic cells predict hippocampal volume as a function of HIV status.Journal of neurovirology · 2023Article
- Myelin regulatory factor is a target of individual and interactive effects of HIV-1 Tat and morphine in the striatum and pre-frontal cortex.Journal of neurovirology · 2023Article
- Astrocytes: Role in pathogenesis and effect of commonly misused drugs in the HIV infected brain.Current research in neurobiology · 2023Review
- Synaptic dysfunction is associated with alterations in the initiation of goal-directed behaviors: Implications for HIV-1-associated apathy.Experimental neurology · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Memory deficits are characteristic of HIV-associated neurocognitive disorders (HAND) and co-occur with hippocampal pathology. The HIV-1 transactivator of transcription (Tat), a regulatory protein, plays a significant role in these events, but the cellular mechanisms involved are poorly understood. Within the hippocampus, diverse populations of interneurons form complex networks; even subtle disruptions can drastically alter synaptic output, resulting in behavioral dysfunction. We hypothesized that HIV-1 Tat would impair cognitive behavior and injure specific hippocampal interneuron subtypes. Male transgenic mice that inducibly expressed HIV-1 Tat (or non-expressing controls) were assessed for cognitive behavior or had hippocampal CA1 subregions evaluated via interneuron subpopulation markers. Tat exposure decreased spatial memory in a Barnes maze and mnemonic performance in a novel object recognition test. Tat reduced the percentage of neurons expressing neuronal nitric oxide synthase (nNOS) without neuropeptide Y immunoreactivity in the stratum pyramidale and the stratum radiatum, parvalbumin in the stratum pyramidale, and somatostatin in the stratum oriens, which are consistent with reductions in interneuron-specific interneuron type 3 (IS3), bistratified, and oriens-lacunosum-moleculare interneurons, respectively. The findings reveal that an interconnected ensemble of CA1 nNOS-expressing interneurons, the IS3 cells, as well as subpopulations of parvalbumin- and somatostatin-expressing interneurons are preferentially vulnerable to HIV-1 Tat. Importantly, the susceptible interneurons form a microcircuit thought to be involved in feedback inhibition of CA1 pyramidal cells and gating of CA1 pyramidal cell inputs. The identification of vulnerable CA1 hippocampal interneurons may provide novel insight into the basic mechanisms underlying key functional and neurobehavioral deficits associated with HAND.
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