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Mesial Temporal Lobe Epilepsy: Pathogenesis, Induced Rodent Models and Lesions
1 Department of Comparative Pathobiology, Purdue University, West Lafayette, IN 47907, USA Correspondence: Address correspondence to Alok K. Sharma, Department of Pathology, Covance Laboratories Inc., 3301 Kinsman Boulevard, Madison, WI, 53704-2523 USA; e-mail:Alok.Sharma{at}covance.com Mesial temporal lobe epilepsy (MTLE), the most common epilepsy in adults, is generally intractable and is suspected to be the result of recurrent excitation or inhibition circuitry. Recurrent excitation and the development of seizures have been associated with aberrant mossy fiber sprouting in the hippocampus. Of the animal models developed to investigate the pathogenesis of MTLE, post-status epilepticus models have received the greatest acceptance because they are characterized by a latency period, the development of spontaneous motor seizures, and a spectrum of lesions like those of MTLE. Among post-status epilepticus models, induction of systemic kainic acid or pilocarpine-induced epilepsy is less labor-intensive than electrical-stimulation models and these models mirror the clinicopathologic features of MTLE more closely than do kindling, tetanus toxin, hyperthermia, post-traumatic, and perinatal hypoxia/ischemia models. Unfortunately, spontaneous motor seizures do not develop in kindling or adult hyperthermia models and are not a consistent finding in tetanus toxin-induced or perinatal hypoxia/ischemia models. This review presents the mechanistic hypotheses for seizure induction, means of model induction, and associated pathology, especially as compared to MTLE patients. Animal models are valuable tools not only to study the pathogenesis of MTLE, but also to evaluate potential antiepileptogenic drugs.
Key Words: Mesial temporal lobe epilepsy • MTLE • rodent models • hippocampus • seizures • mechanisms • histopathology • lesions Abbreviations: NBQX, 6-nitro-7-sulfamoylbenzo(f)quinoxaline-2,3-dione • AMPA, Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid • AC, Associational commissural pathway • BrdU, Bromodeoxyuridine (5-bromo-2-deoxyuridine) • CA, Cornu ammonis • DG, Dentate gyrus • DS, Dorsal subiculum • EEG, Electroencephalographic • EC, Entorhinal cortex • FPI, Fluid percussion injury • GABA, Gamma-aminobutyric acid • GAD, Glutamic acid decarboxylase • HS, Hippocampal sclerosis • HI, Hypoxia/ischemia • IPSP, Inhibitory post-synaptic potential • i.a., Intra-amygdaloid • i.h., Intra-hippocampal • i.p.p., Intra-perforantpath • i.p., Intra-peritoneal • KA, Kainic acid • LEC, Lateral entorhinal cortex • LPP, Lateral perforant path • MHC, Major histocompatibility complex • MaTLE, Mass-associated temporal lobe epilepsy • MEC, Medial entorhinal cortex • MPP, Medial perforant path • MTLE, Mesial temporal lobe epilepsy • MF, Mossy fiber • NMDA, N-methyl-D-aspartic acid • PTLE, Paradoxical temporal lobe epilepsy • PDS, Paroxysmal depolarization shift • PTZ, Pentylenetetrazole • PP, Perforant path • PHAL, Phaseolus vulgaris leucoagglutinin • RCCA, Right common carotid artery • SC, Schaffer collateral pathway • SE, Status Epilepticus • Sb, Subiculum • TLE, Temporal lobe epilepsy • TUNEL, Terminal transferase dUTP nick end labeling • VS, Ventral subiculum
Toxicologic Pathology, Vol. 35, No. 7,
984-999 (2007) This article has been cited by other articles:
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