Advanced Search

Journal Navigation

Journal Home

Subscriptions

Archive

Contact Us

Table of Contents

Click here to register for free online access

Sign In to gain access to subscriptions and/or personal tools.
Toxicologic Pathology
This Article
Right arrow Free Full Text Free
Right arrow Free Full Text (Free PDF) Free
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Saved Citations
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Request Reprints
Right arrow Add to My Marked Citations
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Right arrow Citing Articles via Scopus
Google Scholar
Right arrow Articles by Sharma, A. K.
Right arrow Articles by Snyder, P. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Sharma, A. K.
Right arrow Articles by Snyder, P. W.
Right arrowPubmed/NCBI databases
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*PILOCARPINE
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Articles

Mesial Temporal Lobe Epilepsy: Pathogenesis, Induced Rodent Models and Lesions

Alok K. Sharma1,3, Rachel Y. Reams2, William H. Jordan2, Margaret A. Miller1, H. Leon Thacker1 and Paul W. Snyder1

1 Department of Comparative Pathobiology, Purdue University, West Lafayette, IN 47907, USA
2 Department of Pathology, Lilly Research Laboratories, Division of Eli Lilly and Co., Greenfield, IN, 46140, USA
3 Department of Pathology, Covance Laboratories Inc., Madison, WI, 53704, 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)
DOI: 10.1080/01926230701748305


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
Toxicol PatholHome page
A. K. Sharma, W. H. Jordan, R. Y. Reams, D. G. Hall, and P. W. Snyder
Temporal Profile of Clinical Signs and Histopathologic Changes in an F-344 Rat Model of Kainic Acid-induced Mesial Temporal Lobe Epilepsy
Toxicol Pathol, December 1, 2008; 36(7): 932 - 943.
[Abstract] [Full Text] [PDF]