ArticleNeurobiology of disease2014
Gabapentin attenuates hyperexcitability in the freeze-lesion model of developmental cortical malformation.
Article in Neurobiology of disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Can glial cells save neurons in epilepsy?Neural regeneration research · 2023Review
- Cortical Parvalbumin-Positive Interneuron Development and Function Are Altered in the APC Conditional Knockout Mouse Model of Infantile and Epileptic Spasms Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
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- 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
- Prolonged prophylactic effects of gabapentin on status epilepticus-induced neocortical injury.Neurobiology of disease · 2020Article
- Repurposed molecules for antiepileptogenesis: Missing an opportunity to prevent epilepsy?Epilepsia · 2020Review
- 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
- Neuron-glia interactions in the pathophysiology of epilepsy.Nature reviews. Neuroscience · 2019Review
- Gabapentin Prevents Progressive Increases in Excitatory Connectivity and Epileptogenesis Following Neocortical Trauma.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Does time heal all wounds? Experimental diffuse traumatic brain injury results in persisting histopathology in the thalamus.Behavioural brain research · 2018Article
- APC conditional knock-out mouse is a model of infantile spasms with elevated neuronal β-catenin levels, neonatal spasms, and chronic seizures.Neurobiology of disease · 2017Article
- Article
- 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
- TRAP-seq Profiling and RNAi-Based Genetic Screens Identify Conserved Glial Genes Required for Adult Drosophila Behavior.Frontiers in molecular neuroscience · 2016Article
- Adolescent Intermittent Alcohol Exposure: Dysregulation of Thrombospondins and Synapse Formation are Associated with Decreased Neuronal Density in the Adult Hippocampus.Alcoholism, clinical and experimental research · 2015Article
- Neonatal Seizures: Impact on Neurodevelopmental Outcomes.Frontiers in pediatrics · 2015Review
- 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
- The Evolving View of Astrocytes.Cerebrum : the Dana forum on brain scienceArticle
- Article
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7 authors at 2 institutions in 1 country.
Funding
Abstract
Developmental cortical malformations are associated with a high incidence of drug-resistant epilepsy. The underlying epileptogenic mechanisms, however, are poorly understood. In rodents, cortical malformations can be modeled using neonatal freeze-lesion (FL), which has been shown to cause in vitro cortical hyperexcitability. Here, we investigated the therapeutic potential of gabapentin, a clinically used anticonvulsant and analgesic, in preventing FL-induced in vitro and in vivo hyperexcitability. Gabapentin has been shown to disrupt the interaction of thrombospondin (TSP) with α2δ-1, an auxiliary calcium channel subunit. TSP/α2δ-1 signaling has been shown to drive the formation of excitatory synapses during cortical development and following injury. Gabapentin has been reported to have neuroprotective and anti-epileptogenic effects in other models associated with increased TSP expression and reactive astrocytosis. We found that both TSP and α2δ-1 were transiently upregulated following neonatal FL. We therefore designed a one-week GBP treatment paradigm to block TSP/α2δ-1 signaling during the period of their upregulation. GBP treatment prevented epileptiform activity following FL, as assessed by both glutamate biosensor imaging and field potential recording. GBP also attenuated FL-induced increases in mEPSC frequency at both P7 and 28. Additionally, GBP treated animals had decreased in vivo kainic acid (KA)-induced seizure activity. Taken together these results suggest gabapentin treatment immediately after FL can prevent the formation of a hyperexcitable network and may have therapeutic potential to minimize epileptogenic processes associated with developmental cortical malformations.
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