ArticleNeurobiology of disease2012
Gabapentin decreases epileptiform discharges in a chronic model of neocortical trauma.
Article in Neurobiology of disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 54 citations in OpenAlex.
- Gabapentin and cognitive impairment after traumatic brain injury: A multinational cohort of 49,925 patients.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Advances and challenges in experimental models of posttraumatic epilepsy for therapeutic interventions.Pharmacological reviews · 2025Review
- Agomelatine Alleviates Depressive-like Behaviors by Suppressing Hippocampal Oxidative Stress in the Chronic Social Defeat Stress Model.Antioxidants (Basel, Switzerland) · 2025Article
- New epilepsy therapies in development.Nature reviews. Drug discovery · 2024Review
- Astrocyte Regulation of Synapse Formation, Maturation, and Elimination.Cold Spring Harbor perspectives in biology · 2024Review
- α2δ1-mediated maladaptive sensory plasticity disrupts adipose tissue homeostasis following spinal cord injury.Cell reports. Medicine · 2024Article
- Structural and functional abnormalities in thalamic neurons following neocortical focal status epilepticus.Neurobiology of disease · 2023Article
- Post-Traumatic Epilepsy and Comorbidities: Advanced Models, Molecular Mechanisms, Biomarkers, and Novel Therapeutic Interventions.Pharmacological reviews · 2022Review
- Neuropathophysiological Mechanisms and Treatment Strategies for Post-traumatic Epilepsy.Frontiers in molecular neuroscience · 2021Review
- Combination Therapy of Gabapentin and N-Acetylcysteine Against Posttraumatic Epilepsy in Rats.Neurochemical research · 2020Article
- Prolonged prophylactic effects of gabapentin on status epilepticus-induced neocortical injury.Neurobiology of disease · 2020Article
- Partial Activation of TrkB Receptors Corrects Interneuronal Calcium Channel Dysfunction and Reduces Epileptogenic Activity in Neocortex following Injury.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- Axon growth and synaptic function: A balancing act for axonal regeneration and neuronal circuit formation in CNS trauma and disease.Developmental neurobiology · 2020Review
- Repurposed molecules for antiepileptogenesis: Missing an opportunity to prevent epilepsy?Epilepsia · 2020Review
- In search of antiepileptogenic treatments for post-traumatic epilepsy.Neurobiology of disease · 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
- Is Mossy Fiber Sprouting a Potential Therapeutic Target for Epilepsy?Frontiers in neurology · 2018Review
- Structural alterations in fast-spiking GABAergic interneurons in a model of posttraumatic neocortical epileptogenesis.Neurobiology of disease · 2017Article
- Early Gabapentin Treatment during the Latency Period Increases Convulsive Threshold, Reduces Microglial Activation and Macrophage Infiltration in the Lithium-Pilocarpine Model of Epilepsy.Pharmaceuticals (Basel, Switzerland) · 2017Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Gabapentin (GBP) is an anticonvulsant that acts at the α2δ-1 submit of the L-type calcium channel. It is recently reported that GBP is a potent inhibitor of thrombospondin (TSP)-induced excitatory synapse formation in vitro and in vivo. Here we studied effects of chronic GBP administration on epileptogenesis in the partial cortical isolation ("undercut") model of posttraumatic epilepsy, in which abnormal axonal sprouting and aberrant synaptogenesis contribute to occurrence of epileptiform discharges. Results showed that 1) the incidence of evoked epileptiform discharges in undercut cortical slices studied 1 day or ~2 weeks after the last GBP dose, was significantly reduced by GBP treatments, beginning on the day of injury; 2) the expression of GFAP and TSP1 protein, as well as the number of FJC stained cells was decreased in GBP treated undercut animals; 3) in vivo GBP treatment of rats with undercuts for 3 or 7 days decreased the density of vGlut1-PSD95 close appositions (presumed synapses) in comparison to saline treated controls with similar lesions;4) the electrophysiological data are compatible with the above anatomical changes, showing decreases in mEPSC and sEPSC frequency in the GBP treated animals. These results indicate that chronic administration of GBP after cortical injury is antiepileptogenic in the undercut model of post-traumatic epilepsy, perhaps by both neuroprotective actions and decreases in excitatory synapse formation. The findings may suggest the potential use of GBP as an antiepileptogenic agent following traumatic brain injury.
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