ArticleGlia2020
Toxoplasma infection induces microglia-neuron contact and the loss of perisomatic inhibitory synapses.
Article in Glia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 54 citations in OpenAlex.
- Glial-neuronal crosstalk via GABA signaling: mechanistic insights into neuropsychiatric and neurological pathophysiology.Molecular psychiatry · 2026Review
- Targeting the cGAS-STING pathway alleviates neuroinflammation and cognitive impairment induced by chronic infection of Toxoplasma gondii.Journal of neuroinflammation · 2026Article
- Article
- Possible association between Toxoplasma gondii infection and autism spectrum disorder.Parasites, hosts and diseases · 2025Review
- Review: Gut Microbiota-A Powerful Tool for Improving Pig Welfare by Influencing Behavior Through the Gut-Brain Axis.Animals : an open access journal from MDPI · 2025Review
- Cytoskeletal alterations in neuronal cells implicate Toxoplasma gondii secretory machinery and host microRNA-containing extracellular vesicles.Scientific reports · 2025Article
- Review
- Current perspectives on microglia-neuron communication in the central nervous system: Direct and indirect modes of interaction.Journal of advanced research · 2024Review
- Complement-dependent loss of inhibitory synapses on pyramidal neurons following Toxoplasma gondii infection.Journal of neurochemistry · 2024Article
- Human Brain In Vitro Model for Pathogen Infection-Related Neurodegeneration Study.International journal of molecular sciences · 2024Review
- Microglia in Ischemic Stroke: Pathogenesis Insights and Therapeutic Challenges.Journal of inflammation research · 2024Review
- Lentinan has a beneficial effect on cognitive deficits induced by chronic Toxoplasma gondii infection in mice.Parasites & vectors · 2023Article
- Human brain microphysiological systems in the study of neuroinfectious disorders.Experimental neurology · 2023Review
- Chronic infection by atypicalBrain, behavior, & immunity - health · 2023Article
- Latent toxoplasmosis impairs learning and memory yet strengthens short-term and long-term hippocampal synaptic plasticity at perforant pathway-dentate gyrus, and Schaffer collatterals-CA1 synapses.Scientific reports · 2023Article
- β-Glucan alleviates goal-directed behavioral deficits in mice infected with Toxoplasma gondii.Parasites & vectors · 2023Article
- Use ofFrontiers in cellular and infection microbiology · 2023Review
- New insight in the cross-talk between microglia and schizophrenia: From the perspective of neurodevelopment.Frontiers in psychiatry · 2023Review
- The Defensive Interactions of Prominent Infectious Protozoan Parasites: The Host's Complement System.Biomolecules · 2022Review
- Understanding neuroinflammation through central nervous system infections.Current opinion in neurobiology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Infection and inflammation within the brain induces changes in neuronal connectivity and function. The intracellular protozoan parasite, Toxoplasma gondii, is one pathogen that infects the brain and can cause encephalitis and seizures. Persistent infection by this parasite is also associated with behavioral alterations and an increased risk for developing psychiatric illness, including schizophrenia. Current evidence from studies in humans and mouse models suggest that both seizures and schizophrenia result from a loss or dysfunction of inhibitory synapses. In line with this, we recently reported that persistent T. gondii infection alters the distribution of glutamic acid decarboxylase 67 (GAD67), an enzyme that catalyzes GABA synthesis in inhibitory synapses. These changes could reflect a redistribution of presynaptic machinery in inhibitory neurons or a loss of inhibitory nerve terminals. To directly assess the latter possibility, we employed serial block face scanning electron microscopy (SBFSEM) and quantified inhibitory perisomatic synapses in neocortex and hippocampus following parasitic infection. Not only did persistent infection lead to a significant loss of perisomatic synapses, it induced the ensheathment of neuronal somata by myeloid-derived cells. Immunohistochemical, genetic, and ultrastructural analyses revealed that these myeloid-derived cells included activated microglia. Finally, ultrastructural analysis identified myeloid-derived cells enveloping perisomatic nerve terminals, suggesting they may actively displace or phagocytose synaptic elements. Thus, these results suggest that activated microglia contribute to perisomatic inhibitory synapse loss following parasitic infection and offer a novel mechanism as to how persistent T. gondii infection may contribute to both seizures and psychiatric illness.
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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.