Retinal function in brain death: ERG and oscillatory potentials recording

1997 ◽  
Vol 103 (1) ◽  
pp. 188
Author(s):  
A Polo
Keyword(s):  
Brain Death ◽  
Oscillatory Potentials ◽  
Retinal Function

S-Adenosyl-l-methionine restores photoreceptor function following acute retinal ischemia

2009 ◽  
Vol 26 (5-6) ◽  
pp. 429-441 ◽  
Author(s):  
LEITH MOXON-LESTER ◽  
KEI TAKAMOTO ◽  
PAUL B. COLDITZ ◽  
NIGEL L. BARNETT
Keyword(s):  
Creatine Kinase ◽  
Ischemia Reperfusion ◽  
Oscillatory Potentials ◽  
Retinal Ischemia ◽  
Creatine Kinase Activity ◽  
Retinal Function ◽  
Ischemic Insult ◽  
Adult Rats ◽  
Neuroprotective Strategy ◽  
And Function

AbstractThe survival and function of retinal neurons is dependent on mitochondrial energy generation and its intracellular distribution by creatine kinase. Post ischemic disruption of retinal creatine synthesis, creatine kinase activity, or transport of creatine into neurons may impair retinal function. S-adenosyl-l-methionine (SAMe) is required for creatine synthesis, phosphatidylcholine and glutathione synthesis, and transducin methylation. These reactions are essential for photoreceptor function but may be downregulated after ischemia due to a reduction in SAMe. Our aim was to determine whether administration of SAMe after ischemia could improve retinal function. Unilateral retinal ischemia was induced in adult rats by increasing the intraocular pressure to 110 mm Hg for 60 min. Immediately after the ischemic insult, SAMe was injected into the vitreous (100μm), followed by oral administration (69 mg/kg/day) for 5 or 10 days. Retinal function (electroretinography), histology, and creatine transporter (CRT-1) expression were analyzed. Photoreceptoral responses (RmP3,S), rod and cone bipolar cell responses (PII), and oscillatory potentials were reduced by the ischemia/reperfusion insult. Although SAMe treatment ameliorated the ischemia-induced histological damage by day 5, there was no improvement in retinal function and the intensity of CRT-1 labeling in ischemic retinas was markedly reduced. However, 10 days after ischemia, a recovery in CRT-1 immunolabeling was evident and SAMe supplementation significantly restored photoreceptor function and rod PII responses. In conclusion, these data suggest that creatine transport and methylation reactions, such as creatine synthesis, may be compromised by an ischemic insult contributing to retinal dysfunction and injury. Oral SAMe supplementation after retinal ischemia may provide an effective, safe, and accessible neuroprotective strategy.

Multifocal and full-field electroretinogram changes associated with color-vision loss in mercury vapor exposure

2004 ◽  
Vol 21 (3) ◽  
pp. 421-429 ◽  
Author(s):  
DORA F. VENTURA ◽  
MARCELO T.V. COSTA ◽  
MARCELO F. COSTA ◽  
ADRIANA BEREZOVSKY ◽  
SOLANGE R. SALOMÃO ◽  
...  
Keyword(s):  
Color Vision ◽  
Vision Loss ◽  
Color Discrimination ◽  
Mercury Vapor ◽  
Oscillatory Potentials ◽  
Retinal Function ◽  
Mercury Contamination ◽  
Central Field ◽  
Full Field ◽  
Color Vision Loss

We evaluated the color vision of mercury-contaminated patients and investigated possible retinal origins of losses using electroretinography. Participants were retired workers from a fluorescent lamp industry diagnosed with mercury contamination (n= 43) and age-matched controls (n= 21). Color discrimination was assessed with the Cambridge Colour Test (CCT). Retinal function was evaluated by using the ISCEV protocol for full-field electroretinography (full-field ERG), as well as by means of multifocal electroretinography (mfERG). Color-vision losses assessed by the CCT consisted of higher color-discrimination thresholds along the protan, deutan, and tritan axes and significantly larger discrimination ellipses in mercury-exposed patients compared to controls. Full-field ERG amplitudes from patients were smaller than those of the controls for the scotopic responseb-wave, maximum response, sum of oscillatory potentials (OPs), 30-Hz flicker response, and light-adapted cone response. OP amplitudes measured in patients were smaller than those of controls for O2 and O3. Multifocal ERGs recorded from ten randomly selected patients showed smaller N1–P1 amplitudes and longer latencies throughout the 25-deg central field. Full-field ERGs showed that scotopic, photopic, peripheral, and midperipheral retinal functions were affected, and the mfERGs indicated that central retinal function was also significantly depressed. To our knowledge, this is the first demonstration of retinal involvement in visual losses caused by mercury toxicity.

scholarly journals Evaluation of inner retinal function in myopia using oscillatory potentials of the multifocal electroretinogram

2006 ◽  
Vol 46 (24) ◽  
pp. 4096-4103 ◽  
Author(s):  
Jennifer C. Chen ◽  
Brian Brown ◽  
Katrina L. Schmid
Keyword(s):  
Multifocal Electroretinogram ◽  
Oscillatory Potentials ◽  
Retinal Function

Dose-dependent effects of 6-hydroxy dopamine on deprivation myopia, electroretinograms, and dopaminergic amacrine cells in chickens

1992 ◽  
Vol 9 (5) ◽  
pp. 483-492 ◽  
Author(s):  
Xiao-Xin Li ◽  
Frank Schaeffel ◽  
Konrad Kohler ◽  
Eberhart Zrenner
Keyword(s):  
Monoclonal Antibody ◽  
Tyrosine Hydroxylase ◽  
Intravitreal Injection ◽  
Spectral Sensitivity ◽  
Amacrine Cells ◽  
Oscillatory Potentials ◽  
Retinal Function ◽  
Dose Dependent ◽  
Higher Doses ◽  
Dopaminergic Pathways

AbstractWe found that a single intravitreal injection of 6-hydroxy dopamine (6-OHDA) is highly efficient in blocking the development of deprivation-induced myopia in young chickens. To investigate the effects of 6-OHDA on retinal function, we studied electroretinograms (ERGs) in chickens aged 15-25 days, 4 days subsequent to the injection. Both spectral sensitivity and oscillatory potentials were tested. In addition, a histological examination was performed of dopaminergic amacrine cells labeled by a monoclonal antibody against tyrosine hydroxylase. We found that, at doses of 6-OHDA sufficient to suppress deprivation myopia entirely, no effect could be detected on either the ERGs or on the density and appearance of dopaminergic amacrine cells. For higher doses, spectral sensitivity and the number of dopaminergic amacrine cells declined gradually. In contrast, as doses increased, oscillatory potentials 1 and 2 grew in amplitude only to decline at the highest doses. The results indicate that (1) development of deprivation myopia requires normal retinal function and that (2) slight changes in the gains of dopaminergic pathways are sufficient to block the development of deprivation myopia.

Brain Death: Physiologic Definitions

1985 ◽  
Vol 1 (2) ◽  
pp. 375-396 ◽  
Author(s):  
Nancy Setzer
Keyword(s):  
Brain Death
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