ArticleBritish journal of pharmacology1999
Modification of membrane currents in mouse neuroblastoma cells following infection with rabies virus.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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26 citing papers in PubMed, 60 citations in OpenAlex.
- Induced expression of rabies glycoprotein in the dorsal hippocampus enhances hippocampal dependent memory in a rat model of Alzheimer's disease.Journal of neurovirology · 2024Article
- Acute Adenoviral Infection Elicits an Arrhythmogenic Substrate Prior to Myocarditis.Circulation research · 2024Article
- Lentiviral Expression of Rabies Virus Glycoprotein in the Rat Hippocampus Strengthens Synaptic Plasticity.Cellular and molecular neurobiology · 2022Article
- Eastern equine encephalitis virus rapidly infects and disseminates in the brain and spinal cord of cynomolgus macaques following aerosol challenge.PLoS neglected tropical diseases · 2022Article
- Establishment of Human-Induced Pluripotent Stem Cell-Derived Neurons-A Promising In Vitro Model for a Molecular Study of Rabies Virus and Host Interaction.International journal of molecular sciences · 2021Article
- Rabies virus glycoprotein enhances spatial memory via the PDZ binding motif.Journal of neurovirology · 2021Article
- Early Transcriptional Changes in Rabies Virus-Infected Neurons and Their Impact on Neuronal Functions.Frontiers in microbiology · 2021Article
- Quantitative Proteome Profiling of Street Rabies Virus-Infected Mouse Hippocampal Synaptosomes.Current microbiology · 2016Article
- Perspectives in Diagnosis and Treatment of Rabies Viral Encephalitis: Insights from Pathogenesis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2016Review
- Systems Biomedicine of Rabies Delineates the Affected Signaling Pathways.Frontiers in microbiology · 2016Article
- Genome-Wide Transcriptional Profiling Reveals Two Distinct Outcomes in Central Nervous System Infections of Rabies Virus.Frontiers in microbiology · 2016Article
- Novel Approaches to the Prevention and Treatment of Rabies.International journal of virology studies & research · 2015Article
- Synaptic Plasticity and Neurological Disorders in Neurotropic Viral Infections.Neural plasticity · 2015Review
- Street rabies virus causes dendritic injury and F-actin depolymerization in the hippocampus.The Journal of general virology · 2013Article
- Immune clearance of attenuated rabies virus results in neuronal survival with altered gene expression.PLoS pathogens · 2012Article
- Update on rabies.Research and reports in tropical medicine · 2011Review
- Concepts in the pathogenesis of rabies.Future virology · 2008Article
- Structural abnormalities in neurons are sufficient to explain the clinical disease and fatal outcome of experimental rabies in yellow fluorescent protein-expressing transgenic mice.Journal of virology · 2008Article
- Mechanisms of escape phenomenon of spinal cord and brainstem in human rabies.BMC infectious diseases · 2005Article
- Degeneration of neuronal processes after infection with pathogenic, but not attenuated, rabies viruses.Journal of virology · 2005Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effect on membrane currents of infection of mouse neuroblastoma NA cells with rabies virus was studied by using the whole-cell patch clamp technique. 2. Three types of membrane currents, namely voltage-dependent Na+ current (I(Na)), delayed rectifier K+ current (I(K-DR)) and inward rectifier K+ current (I(K-IR)) were elicited in uninfected cells. 3. In cells 3 days after infection with the virus, no detectable change was observed in morphology and membrane capacitance, but I(Na) and I(K-IR) were significantly decreased in amplitude without any appreciable difference in the time course of current activation and inactivation. The voltage-dependence of I(Na) activation was significantly shifted in the positive direction along the voltage axis with a decreased slope. I(K-DR) remained almost unaltered after the viral infection. 4. The resting membrane potential, measured with a physiological K+ gradient across the cell membrane, was decreased (depolarized) after the viral infection. The depolarization was associated with the decreased amplitude of I(K-IR). 5. These results suggest that infection of mouse neuroblastoma NA cells with rabies virus causes reduction of functional expression of ion channels responsible for I(Na) and I(K-IR), and provide evidence for possible involvement of the change in membrane properties in the pathogenesis of rabies disease.
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