An Electrophysiological Study of Retinal Function in the Diabetic Female Rat

Abstract

The results suggest that changes in the GABA-signaling pathway may be the underlying cellular mechanism for altered ERG responses in STZ-induced diabetes in rats. Recognition of these early neurosensory defects would enable a better understanding of the pathophysiological basis of diabetic retinopathy.

Critical role of endoplasmic reticulum stress in chronic endothelial activation−induced visual deficits in tie2‐tumor necrosis factor mice

“…Our results in this study demonstrate significantly lower b‐wave amplitudes in tie2‐TNF mice at 3 months of age, suggesting retinal damage in this model. On the other hand, diabetic tie2‐TNF mice demonstrated a further decrease in ERG amplitudes, which is in agreement with previously reported data in diabetic rodent models . A number of reasons could be considered for the observed visual deficits in our mice.…”

Critical role of endoplasmic reticulum stress in chronic endothelial activation−induced visual deficits in tie2‐tumor necrosis factor mice

“…Our results in this study demonstrate significantly lower b‐wave amplitudes in tie2‐TNF mice at 3 months of age, suggesting retinal damage in this model. On the other hand, diabetic tie2‐TNF mice demonstrated a further decrease in ERG amplitudes, which is in agreement with previously reported data in diabetic rodent models . A number of reasons could be considered for the observed visual deficits in our mice.…”

Featured Article: Deterioration of visual function mediated by senescence-associated endoplasmic reticulum stress in inflammatory tie2-TNF mice

“…It is interesting to note that visual deficits seen in TNF mice increased in an age-dependent fashion, with animals 10 months old showing more defects when compared with those five months of age. Both ERG and OKN defects observed in the model are consistent with other rodent models that display inflammation, 52 ER stress, 53 neurotransmitter defects, 54 or retinal microcirculation, 55,56 all of which are correlated with premature cellular senescence and/or ER stress pathways. Specifically, inflammation and oxidative stress have been linked to outer retinal defects, with photoreceptors having the highest susceptibility to oxidative damage.…”

Functional alterations of retinal neurons and vascular involvement progress simultaneously in the Psammomys obesus model of diabetic retinopathy

“…We found that 3 months of diabetes in P. obesus did not affect the amplitude of the scotopic a-wave although a significant decrease involved in the genesis of the rod-mediated b-wave, were the first affected by the diabetes-induced retinopathy, a finding that confirms previous immunohistological report (Baccouche et al, 2018). Normal a-wave has been reported in diabetic humans with type 1 diabetes even without clinical signs, suggesting that Müller cell's reactivity and rod bipolar cells alteration symptoms (Lovasik & Kergoat, 1993) and treated Long-Evans rats (Hancock & Kraft, 2004;Ramsey et al, 2006).…”

Critical role of endoplasmic reticulum stress in chronic endothelial activation−induced visual deficits in tie2‐tumor necrosis factor mice

“…Our results in this study demonstrate significantly lower b‐wave amplitudes in tie2‐TNF mice at 3 months of age, suggesting retinal damage in this model. On the other hand, diabetic tie2‐TNF mice demonstrated a further decrease in ERG amplitudes, which is in agreement with previously reported data in diabetic rodent models . A number of reasons could be considered for the observed visual deficits in our mice.…”

Featured Article: Deterioration of visual function mediated by senescence-associated endoplasmic reticulum stress in inflammatory tie2-TNF mice

“…It is interesting to note that visual deficits seen in TNF mice increased in an age-dependent fashion, with animals 10 months old showing more defects when compared with those five months of age. Both ERG and OKN defects observed in the model are consistent with other rodent models that display inflammation, 52 ER stress, 53 neurotransmitter defects, 54 or retinal microcirculation, 55,56 all of which are correlated with premature cellular senescence and/or ER stress pathways. Specifically, inflammation and oxidative stress have been linked to outer retinal defects, with photoreceptors having the highest susceptibility to oxidative damage.…”

Functional alterations of retinal neurons and vascular involvement progress simultaneously in the Psammomys obesus model of diabetic retinopathy

“…We found that 3 months of diabetes in P. obesus did not affect the amplitude of the scotopic a-wave although a significant decrease involved in the genesis of the rod-mediated b-wave, were the first affected by the diabetes-induced retinopathy, a finding that confirms previous immunohistological report (Baccouche et al, 2018). Normal a-wave has been reported in diabetic humans with type 1 diabetes even without clinical signs, suggesting that Müller cell's reactivity and rod bipolar cells alteration symptoms (Lovasik & Kergoat, 1993) and treated Long-Evans rats (Hancock & Kraft, 2004;Ramsey et al, 2006).…”

Critical role of endoplasmic reticulum stress in chronic endothelial activation−induced visual deficits in tie2‐tumor necrosis factor mice

“…Our results in this study demonstrate significantly lower b‐wave amplitudes in tie2‐TNF mice at 3 months of age, suggesting retinal damage in this model. On the other hand, diabetic tie2‐TNF mice demonstrated a further decrease in ERG amplitudes, which is in agreement with previously reported data in diabetic rodent models . A number of reasons could be considered for the observed visual deficits in our mice.…”

Featured Article: Deterioration of visual function mediated by senescence-associated endoplasmic reticulum stress in inflammatory tie2-TNF mice

“…It is interesting to note that visual deficits seen in TNF mice increased in an age-dependent fashion, with animals 10 months old showing more defects when compared with those five months of age. Both ERG and OKN defects observed in the model are consistent with other rodent models that display inflammation, 52 ER stress, 53 neurotransmitter defects, 54 or retinal microcirculation, 55,56 all of which are correlated with premature cellular senescence and/or ER stress pathways. Specifically, inflammation and oxidative stress have been linked to outer retinal defects, with photoreceptors having the highest susceptibility to oxidative damage.…”

Functional alterations of retinal neurons and vascular involvement progress simultaneously in the Psammomys obesus model of diabetic retinopathy

“…We found that 3 months of diabetes in P. obesus did not affect the amplitude of the scotopic a-wave although a significant decrease involved in the genesis of the rod-mediated b-wave, were the first affected by the diabetes-induced retinopathy, a finding that confirms previous immunohistological report (Baccouche et al, 2018). Normal a-wave has been reported in diabetic humans with type 1 diabetes even without clinical signs, suggesting that Müller cell's reactivity and rod bipolar cells alteration symptoms (Lovasik & Kergoat, 1993) and treated Long-Evans rats (Hancock & Kraft, 2004;Ramsey et al, 2006).…”