Document Detail


Review of the role of inhibitory neurons in chronic epileptic foci induced by intracerebral tetanus toxin.
MedLine Citation:
PMID:  8985687     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Blocking inhibition provides one of the most common experimental means of triggering epileptic activity in hippocampus and neocortex. However, it has proved much more difficult to show that chronic models of epilepsies are due to disinhibition. One problem is knowing how much inhibition needs to be blocked to provide a sufficient mechanism for epileptic activity. We have found that inhibitory (GABAA) transmission, estimated from evoked monosynaptic IPSCs, must be reduced to 17% of their control amplitude (by 4-7 microM bicuculline) before hippocampal slices generate all-or-none epileptic discharges. Similar estimates of inhibition in chronic epileptic foci induced by intrahippocampal injection of tetanus toxin showed that monosynaptic IPSCs dropped to 10% of control in the injected hippocampus during the first 2 weeks after injection. At all other stages of the active epileptic foci in the two hippocampi the reduction in IPSCs was not alone sufficient for epileptic activity; at 4-6 weeks IPSCs were normal despite continued epileptic activity. One likely mechanism for the late epileptic activity is a reduction of either the intrinsic excitability, or the synaptic excitation, of inhibitory interneurons so they fail to be recruited normally. Alternative mechanisms include the formation of new excitatory connections, as found at modest levels in the dentate gyrus. Several mechanisms may play a part in chronic foci such as those induced by tetanus toxin, either acting together, or sequentially during the progression of the epileptic focus.
Authors:
J G Jefferys; M A Whittington
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Epilepsy research     Volume:  26     ISSN:  0920-1211     ISO Abbreviation:  Epilepsy Res.     Publication Date:  1996 Dec 
Date Detail:
Created Date:  1997-04-14     Completed Date:  1997-04-14     Revised Date:  2009-09-29    
Medline Journal Info:
Nlm Unique ID:  8703089     Medline TA:  Epilepsy Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  59-66     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of Birmingham, UK. j.g.r.jefferys@bham.ac.uk
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MeSH Terms
Descriptor/Qualifier:
6-Cyano-7-nitroquinoxaline-2,3-dione / pharmacology
Animals
Bicuculline / pharmacology
Cerebral Cortex / drug effects,  physiopathology
Disease Models, Animal
Epilepsy / chemically induced*,  physiopathology
Functional Laterality / drug effects
Hippocampus / drug effects,  physiopathology*
Interneurons / drug effects,  physiology
Male
Neural Inhibition / drug effects*,  physiology
Rats
Rats, Sprague-Dawley
Synaptic Transmission / drug effects,  physiology
Tetanus Toxin* / pharmacology
gamma-Aminobutyric Acid / physiology
Grant Support
ID/Acronym/Agency:
//Wellcome Trust
Chemical
Reg. No./Substance:
0/Tetanus Toxin; 115066-14-3/6-Cyano-7-nitroquinoxaline-2,3-dione; 485-49-4/Bicuculline; 56-12-2/gamma-Aminobutyric Acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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