The Rentería Lab is working to understand the pathophysiology of diabetic retinopathy, a major complication of diabetes and leading cause of blindness. Chronic injuries to vascular cells and to neurons interact to cause disease progression. Using techniques including single- and multi-electrode electrophysiology, immunohistochemistry, protein biochemistry, and tests of visual behavior in rodents, we aim to uncover new treatment strategies based on understanding of these injury mechanisms.
In a second project, we seek to understand how activity shapes the circuitry and neural output of the mammalian retina during both normal postnatal development and development after hypoxic and ischemic insults, again using rodents as our model system.
We also aim to discover the influence of retinal function on the performance of specific visual behaviors.
Akimov NP, Rentería RC. Dark rearing alters the normal development of spatiotemporalresponse properties but not of contrast detection threshold in mouse retinalganglion cells. Dev Neurobiol. 2014 Jan 10.
Muir ER, Rentería RC, Duong TQ. Reduced ocular blood flow as an early indicator of diabeticretinopathy in a mouse model of diabetes. Invest Ophthalmol Vis Sci. 2012 Sep 21;53(10):6488-94.
Akimov NP, Rentería RC. Spatial frequency threshold and contrast sensitivity of anoptomotor behavior are impaired in the Ins2Akita mouse model of diabetes. Behav Brain Res. 2012 Jan 15;226(2):601-5.
Barabas P, Huang W, Chen H, Koehler CL, Howell G, John SW, Tian N, Rentería RC, Krizaj D. Missing optomotor head-turning reflex in the DBA/2J mouse. Invest Ophthalmol Vis Sci. 2011 Aug 29;52(9):6766-73.
Koehler CL, Akimov NP, Rentería RC. Receptive field center size decreases and firing properties mature in ON andOFF retinal ganglion cells after eye opening in the mouse. J Neurophysiol. 2011 Aug;106(2):895-904.