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JCI online early table of contents: July 12, 2010
Date:7/12/2010

e in CpG elicit vigorous CD4+ T cell responses against blood-stage malaria in mice

AUTHOR CONTACT:
Michael F. Good
Queensland Institute of Medical Research, Brisbane, Queensland, Australia.
Phone: 61.7.3362.0203; Fax: 61.7.3362.0110; E-mail: Michael.Good@qimr.edu.au.

View this article at: http://www.jci.org/articles/view/39222?key=c05c1cb488663ceb3c72


NEUROBIOLOGY: Protein mislocalization gets nerve cells all excited

Individuals with the childhood epilepsy syndrome genetic epilepsy with febrile seizures plus (GEFS+) suffer generalized epilepsies of variable severity and febrile seizures, which are convulsions brought on by a fever. GEFS+ is often associated with genetic mutations that alter the function of proteins known as sodium channels. To investigate how such mutations cause the symptoms of GEFS+, a team of researchers, led by Steven Petrou, at The University of Melbourne, Australia, generated mice expressing one copy of a mutated gene associated with GEFS+ in humans. This gene made a C121W mutant version of the beta-1 sodium channel accessory subunit protein. Detailed analysis of the mice led the team to conclude that the beta-1 sodium channel accessory subunit protein normally modulates the excitability of regions of pyramidal nerve cells known as the axon initial segments and that the C121W mutant protein was excluded from such regions, thereby disrupting the regulation of axon initial segment excitability and causing epilepsy.

TITLE: Axon initial segment dysfunction in a mouse model of genetic epilepsy with febrile seizures plus

AUTHOR CONTACT:
Steven Petrou
The University of Melbourne, Parkville, Victoria, Australia.
Phone: 61.3.83441957; Fax: 61.3.93470446; E-mail: spetrou@unimelb.edu.au'/>"/>

Contact: Karen Honey
press_releases@the-jci.org
734-546-5242
Journal of Clinical Investigation
Source:Eurekalert

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