Epilepsy
Translational In Vivo Models for Testing Novel AEDs
Epilepsy
Epilepsy, one of the most prevalent neurological disorders that affects approximately 65 million individuals globally, is characterized by a tendency for recurrent seizures. Despite advancements in new antiepileptic drugs (AEDs), the pursuit of more effective and tolerable therapies remains a significant challenge. Numerous models of epilepsy and seizures have been developed for preclinical epilepsy research and the discovery of AEDs. Utilize our array of translational in vivo epilepsy models and experienced scientists to test your novel therapeutic.
Animal Models of Epilepsy
We have established various mouse and rat models for preclinical epilepsy research and drug discovery. The selection of appropriate animal models is crucial in aligning with the developmental stages and experimental goals in the discovery and development of new AEDs.
Acute Seizure Models
Model Summary
Acute seizure rodent models play a crucial role in the early stages of drug development. These models allow researchers to observe and measure seizure characteristics, such as severity and duration, and are instrumental in the initial screening of potential AEDs for their efficacy in mitigating acute seizures. We utilize pentylenetetrazol (PTZ; subcutaneous [s.c.] or intraperitoneal [i.p.] injection) and N-methyl-D-aspartate (NMDA; i.p. injection) to induce clonic and tonic seizures in mice and rats.
Study Design
Validation Data
Sprague-Dawley rats were either treated with Diaz (10 mg/kg; orange bars) or remained untreated (red bars). Thirty minutes later, all animals were administered PTZ (35 mg/kg) to induce acute seizures. Diaz significantly increased the latency of PTZ-induced seizures and significantly reduced the severity of seizures, as scored on the modified Racine scale. ***p<0.001, n=10.
Temporal Lobe Epilepsy Model
Model Summary
The kainic acid-induced temporal lobe epilepsy (TLE) rodent model involves the administration of kainic acid, an analog of glutamate and potent neurotoxin, to induce seizures that spread through the limbic system, resembling the progression observed in TLE patients. This model replicates key pathological features of human TLE, including hippocampal damage, mossy fiber sprouting, and spontaneous recurrent seizures.
Validation Data
Fluorojade-B staining of degenerating neurons in the rat piriform cortex 4 days after treatment with kainic acid (10 mg/kg, i.p.)
Audiogenic-Induced Epilepsy Model
Genetically Engineered Epilepsy Models
Drug Metabolism and Pharmacokinetics (DMPK)
Histology
Pathology
General Toxicology
Bioanalysis
