Abstracts

FOCAL FREEZE-INDUCED CORTICAL DYSPLASIA IS ASSOCIATED WITH POSTANATAL NEUROGENESIS AND FOCAL CELL MIGRATION

Abstract number : 2.089
Submission category :
Year : 2003
Submission ID : 4097
Source : www.aesnet.org
Presentation date : 12/6/2003 12:00:00 AM
Published date : Dec 1, 2003, 06:00 AM

Authors :
Hiroshi Shigeto, Atthaporn Boongird, Candice Burrier, Berit Jacobson, Christoph Kellighaus, Zhong Ying, Imad Najm Neurology, The Cleveland Clinic Foundation, Cleveland, OH

Recent data show that chemoconvulsant-induced seizures stimulate neurogenesis in the adult rodent dentate gyrus (DG) and rostral migratory stream (RMS). Neurogenesis in SVZ and DG is thought to suggest the possible existence of brain self-repair and restoration of function. However, it is still unknown whether a neocortical focal dysplastic lesion induces neurogenesis. We examined whether a focal freeze lesion in the rodent is associated with neurogenesis and cell migration.
Eight rat pups (PND 1) were used. The lesion was created using a frozen stainless steel probe on the exposed skull of the left hemisphere for 8 seconds. Every 6 hours for the next 24 hours after surgery, all rats were injected with bromodeoxyuridine (BrdU: 50 mg/kg). Four rats were sacrificed 7 days after birth and 4 rats were sacrificed at day 28. Brain tissues were cut into 50mm thick sections and stained using cresylecht violet staining to confirm the presence of the lesion. Immunocytochemical (ICC) staining was performed using anti-BrdU, neuronal (NeuN) and glial (GFAP) antibodies.
All 8 rats had cortical lesions in the left hemisphere, in the location of iced probe contact. Rats sacrificed 7 days after birth displayed a large amount of BrdU positive cells in the SVZ and a moderate amount in the DG and peri-lesional area. As for rats sacrificed at PND 28, BrdU positive cells were increased in number in the peri-lesional area, as compared to rats sacrificed at PND 7. In contrast, BrdU positive cells decreased in number in the SVZ at PND 28. The number of BrdU positive cells in DG did not show significant change between PND 7 and 28. The BrdU positive cells did not exhibit positive ICC staining to mature neuronal or glial markers.
These results suggest that the focal early postnatal freeze-induced dysplastic lesion leads to the activation of neurogenesis and cell migration towards the lesion. The role of postnatal neurogenesis in the formation of focal dysplasia and/or expression of epileptogenicity remain unknown.
[Supported by: Grants from the National Institute of Neurological Disorders and Stroke (NINDS) to IN]