JCI table of contents: June 21, 2007

study appearing online on June 21 in advance of publication in the July print issue of the Journal of Clinical Investigation, Kohichi Tanaka and colleagues from Tokyo Medical and Dental University investigated IOP-independent mechanisms involved in the development of glaucoma. They show that mice deficient in the glutamate transporters GLAST or EAAC1 have spontaneous optical nerve degeneration without elevated IOP. In GLAST-deficient mice, administration of a glutamate receptor blocker prevented optical damage. These animals are believed to be the first animal models of NTG and offer a powerful system for further investigation of retinal degeneration in NTG and the development of therapies directed at preventing or treating IOP-independent glaucoma.

Title: The potential role of glutamate transporters in the pathogenesis of normal tension glaucoma

Author Contact:

Kohichi Tanaka
Tokyo Medical and Dental University, Tokyo, Japan.
Phone : 81-3-5803-5846; Fax:81-3-5803-5843; E-mail: tanaka.aud@mri.tmd.ac.jp

View the PDF of this article at: http://www.the-jci.org/article.php?id=30178


New mouse model for the study of some forms of human hypertension

The angiotensin II receptor, type 1 (AT1) helps control blood pressure; its loss reduces blood pressure, while its overexpression leads to an increase in blood pressure. In a study appearing online on June 21 in advance of publication in the July print issue of the Journal of Clinical Investigation, Eric Clauser and colleagues from Institute Cochin in Paris show that a mutation in AT1 that makes the receptor more sensitive to angiotensin II and the effects of its ligand longer lasting, causes a modest increase in blood pressure, as well as cardiac, vascular, and renal fibrosis, and cardiac dysfunction in mice. This new animal mod

Contact: Brooke Grindlinger
Journal of Clinical Investigation

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