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Logo of bmcgeneBioMed Centralsearchsubmit a manuscriptregisterthis articleBMC Genetics
BMC Genet. 2001; 2: 12.
Published online Aug 9, 2001. doi:  10.1186/1471-2156-2-12
Intraocular pressure in genetically distinct mice: an update and strain survey
Olga V Savinova,1 Fumihiro Sugiyama,2 Janice E Martin,1,3 Stanislav I Tomarev,4 Beverly J Paigen,1 Richard S Smith,1,3 and Simon WM Johncorresponding author1,3,5
1The Jackson Laboratory, 600 Main Street, Bar Harbor, ME, 04609, USA
2Laboratory Animal Resource Center, University of Tsukuba, Tsukuba, 305, Japan
3Howard Hughes Medical Institute at The Jackson Laboratory, 600 Main Street, Bar Harbor, ME, 04609, USA
4Laboratory of Molecular and Developmental Biology, National Eye Institute, NIH, Bethesda, MD, 20892-3655, USA
5Department of Ophthalmology, Tufts University School of Medicine, Boston, MA, 02155, USA
corresponding authorCorresponding author.
Olga V Savinova: ovs/at/; Fumihiro Sugiyama: bunbun/at/; Janice E Martin: jemartin/at/; Stanislav I Tomarev: tomarev/at/; Beverly J Paigen: bjp/at/; Richard S Smith: rss/at/; Simon WM John: swmj/at/
Received June 22, 2001; Accepted August 9, 2001.
Little is known about genetic factors affecting intraocular pressure (IOP) in mice and other mammals. The purpose of this study was to determine the IOPs of genetically distinct mouse strains, assess the effects of factors such as age, sex and time of day on IOP in specific strain backgrounds, and to assess the effects of specific candidate gene mutations on IOP.
Based on over 30 studied mouse strains, average IOP ranges from approximately 10 to 20 mmHg. Gender does not typically affect IOP and aging results in an IOP decrease in some strains. Most tested strains exhibit a diurnal rhythm with IOP being the highest during the dark period of the day. Homozygosity for a null allele of the carbonic anhydrase II gene (Car2n) does not alter IOP while homozygosity for a mutation in the leptin receptor gene (Leprdb) that causes obesity and diabetes results in increased IOP. Albino C57BL/6J mice homozygous for a tyrosinase mutation (Tyrc-2J) have higher IOPs than their pigmented counterparts.
Genetically distinct mouse strains housed in the same environment have a broad range of IOPs. These IOP differences are likely due to interstrain genetic differences that create a powerful resource for studying the regulation of IOP. Age, time of day, obesity and diabetes have effects on mouse IOP similar to those in humans and other species. Mutations in two of the assessed candidate genes (Lepr and Tyr) result in increased IOP. These studies demonstrate that mice are a practical and powerful experimental system to study the genetics of IOP regulation and disease processes that raise IOP to harmful levels.
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