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Hippocampal astrogliosis and neuronal cell loss in an experimental P10 neonatal model of mesial temporal lobe epilepsy.

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posted on 22.11.2019 by Shane Crilly, Mark Dunleavy, David C. Henshall

Mesial temporal lobe epilepsy (MTLE) is the most common form of intractable seizure disorder in adults. It is associated with an asymmetrical pattern of neuron loss within the hilus and CA1 hippocampal subfields, with relative sparing of the dentate granule neurons and the CA2 subfields. The amygdalar nuclei and the cortical neurons are other areas that are rarely involved in MTLE.1

The neuropathological changes that bring about focally evoked seizures in the adult are thought to begin in the early stages of neonatal life. A wide range of factors have been implicated in the causation of MTLE, such as febrile seizures and traumatic brain injury.2 Some studies indicate that up to 74% of those who experience early life status epilepticus develop epilepsy at a later stage.2 The objective of this study is to investigate the neuropathological changes induced by intra-amygdalar kainic acid (KA) microinjection in a postnatal day 10 (P10) rat model of MTLE.3

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This article is also available at http://www.rcsismj.com/wp-content/uploads/RCSIsmj-Vol4-abst-TLE.pdf

Published Citation

Crilly S, Dunleavy M, Henshall DC. Hippocampal astrogliosis and neuronal cell loss in an experimental P10 neonatal model of mesial temporal lobe epilepsy. RCSI Student Medical Journal. 2011;4(1):97-98.

Publication Date

01/01/2011

Publisher

Royal College of Surgeons in Ireland

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