Document Detail


An early decrease in cell proliferation after pentylenetetrazole-induced seizures.
MedLine Citation:
PMID:  21907628     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
There are increasing data on the influence of seizures on neurogenesis in the adult brain. However, data on cell proliferation and differentiation during the early stages of kindling are scarce. We have used pentylenetetrazole (PTZ)-induced kindling to investigate the temporal profile of cytogenesis in the germinative zones of adult rat brain. For comparison, we also used a single PTZ-induced generalized tonic-clonic seizure. During kindling development, the density of 5-bromo-2'-deoxyuridine-positive cells demonstrated similar changes in all germinative zones: a dramatic decrease after the first subthreshold PTZ injection, and a gradual increase to the control level following repeated PTZ administration. On the contrary, a single PTZ-induced generalized tonic-clonic seizure was followed by an increase in the number of proliferating cells in both the dentate gyrus and the subventricular zone. These results may indicate the existence of global mechanisms affecting cellular proliferation in adult brain during seizures. Different temporal profiles of neuronal damage and proliferation changes suggest that neurodegeneration is unlikely to be a global proliferation-regulating factor. The data may contribute to better understanding of the initial phase of kindling development and epileptogenesis.
Authors:
V A Aniol; M Yu Stepanichev; N A Lazareva; N V Gulyaeva
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-9-8
Journal Detail:
Title:  Epilepsy & behavior : E&B     Volume:  -     ISSN:  1525-5069     ISO Abbreviation:  -     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-9-12     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100892858     Medline TA:  Epilepsy Behav     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2011 Elsevier Inc. All rights reserved.
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