Hyperoxia, hyperglycemia, and photoreceptor sensitivity in normal and diabetic subjects.

The aim of this study was to investigate the effects of an increase in the saturation of blood oxygen (SaO2) and/or serum glucose on photoreceptor sensitivity in normal subjects and in patients with diabetes mellitus. We monitored cone and rod sensitivity by recording dark-adaptation curves to both green and red test stimuli while inhaling either air (20% O2 + 80% N2) or 100% oxygen in 12 normal subjects and 12 diabetic patients with no (10) or mild (2) retinopathy. We also repeated the experiment in 10 of the normal subjects under hyperglycemia (mean serum glucose: 161 mg/dl).

MfERG waveform characteristics in the RS1h mouse model featuring a 'negative' ERG.

Several retinal disorders lead to a relatively greater attenuation of the b-wave compared to the a-wave of the electroretinogram (ERG), a constellation called 'negative' ERG. To determine the waveform characteristics of multifocal ERGs (mfERGs) and their dependence on recording parameters in such a case, we studied the Rs1h(-/Y) mouse, the model for x-linked juvenile retinoschisis. mfERGs were recorded with a VERIS 4 system connected to a piggyback stimulator prototype that added the stimulus to the optical pathway of a HRA scanning-laser ophthalmoscope (SLO) by means of a wavelength-sensitive mirror.

cGMP-dependent protein kinase II modulates mPer1 and mPer2 gene induction and influences phase shifts of the circadian clock.

Background: In mammals, the master circadian clock that drives many biochemical, physiological, and behavioral rhythms is located in the suprachiasmatic nuclei (SCN) of the hypothalamus. Generation and maintenance of circadian rhythmicity rely on complex interlocked transcriptional/translational feedback loops involving a set of clock genes. Among the molecular components driving the mammalian circadian clock are the Period 1 and 2 (mPer1 and mPer2) genes.

HIF-1-induced erythropoietin in the hypoxic retina protects against light-induced retinal degeneration.

Erythropoietin (Epo) is upregulated by hypoxia and provides protection against apoptosis of erythroid progenitors in bone marrow and brain neurons. Here we show in the adult mouse retina that acute hypoxia dose-dependently stimulates expression of Epo, fibroblast growth factor 2 and vascular endothelial growth factor via hypoxia-inducible factor-1alpha (HIF-1alpha) stabilization. Hypoxic preconditioning protects retinal morphology and function against light-induced apoptosis by interfering with caspase-1 activation, a downstream event in the intracellular death cascade.