ArticleNeurobiology of disease2013
Glutamate biosensor imaging reveals dysregulation of glutamatergic pathways in a model of developmental cortical malformation.
Article in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Real-time imaging of glutamate transients in the extracellular space of acute human brain slices using a single-wavelength glutamate fluorescence nanosensor.Scientific reports · 2022Article
- Tonic Activation of GluN2C/GluN2D-Containing NMDA Receptors by Ambient Glutamate Facilitates Cortical Interneuron Maturation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Cortical Malformations: Lessons in Human Brain Development.Frontiers in cellular neuroscience · 2019Review
- Astrocyte membrane properties are altered in a rat model of developmental cortical malformation but single-cell astrocytic glutamate uptake is robust.Neurobiology of disease · 2016Article
- Traumatic Brain Injury Increases Cortical Glutamate Network Activity by Compromising GABAergic Control.Cerebral cortex (New York, N.Y. : 1991) · 2015Article
- WONOEP appraisal: molecular and cellular imaging in epilepsy.Epilepsia · 2015Review
- Gabapentin attenuates hyperexcitability in the freeze-lesion model of developmental cortical malformation.Neurobiology of disease · 2014Article
- Excitatory and inhibitory synaptic connectivity to layer V fast-spiking interneurons in the freeze lesion model of cortical microgyria.Journal of neurophysiology · 2014Article
- Article
- Functional changes in glutamate transporters and astrocyte biophysical properties in a rodent model of focal cortical dysplasia.Frontiers in cellular neuroscience · 2014Article
- Laser-scanning astrocyte mapping reveals increased glutamate-responsive domain size and disrupted maturation of glutamate uptake following neonatal cortical freeze-lesion.Frontiers in cellular neuroscience · 2014Article
- Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Cortical malformations can cause intractable epilepsy, but the underlying epileptogenic mechanisms are poorly understood. We used high-speed glutamate biosensor imaging to ask how glutamatergic signaling is altered in cortical malformations induced by neonatal freeze-lesions (FL). In non-lesion neocortical slices from 2 to 8week old rats, evoked glutamate signals were symmetrical in the medio-lateral axis and monotonic, correlating with simple, brief (≈50ms) local field potentials (LFPs). By contrast, in FL cortex glutamate signals were prolonged, increased in amplitude, and polyphasic, which paralleled a prolongation of the LFP. Using glutamate biosensor imaging, we found that glutamate signals propagated throughout large areas of FL cortex and were asymmetric (skewed toward the lesion). Laminar analysis demonstrated a shift in the region of maximal glutamate release toward superficial layers in FL cortex. The ability to remove exogenous glutamate was increased within the FL itself but was decreased in immediately adjacent regions. There were corresponding alterations in astrocyte density, with an increase within the lesion and a decrease in deep cortical layers surrounding the lesion. These findings demonstrate both network connectivity and glutamate metabolism are altered in this cortical malformation model and suggests that the regional ability of astrocytes to remove released glutamate may be inversely related to local excitability.
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