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Enriched Environment Protects the Optic Nerve from Early Diabetes-Induced Damage in Adult Rats.

Dorfman D, Aranda ML, Rosenstein RE - PLoS ONE (2015)

Bottom Line: Diabetic retinopathy is a leading cause of reduced visual acuity and acquired blindness.EE housing which did not affect the STZ-induced weight loss and hyperglycemia, prevented a decrease in the anterograde transport from the retina to the superior colliculus, ON axon number, and phosphorylated neurofilament heavy immunoreactivity.These results suggest that EE induced neuroprotection in the diabetic visual pathway.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Retinal Neurochemistry and Experimental Ophthalmology, Department of Human Biochemistry, School of Medicine/CEFyBO, University of Buenos Aires/CONICET, Buenos Aires, Argentina.

ABSTRACT
Diabetic retinopathy is a leading cause of reduced visual acuity and acquired blindness. Axoglial alterations of the distal (close to the chiasm) optic nerve (ON) could be the first structural change of the visual pathway in streptozotocin (STZ)-induced diabetes in rats. We analyzed the effect of environmental enrichment on axoglial alterations of the ON provoked by experimental diabetes. For this purpose, three days after vehicle or STZ injection, animals were housed in enriched environment (EE) or remained in a standard environment (SE) for 6 weeks. Anterograde transport, retinal morphology, optic nerve axons (toluidine blue staining and phosphorylated neurofilament heavy immunoreactivity), microglia/macrophages (ionized calcium binding adaptor molecule 1 (Iba-1) immunoreactivity), astrocyte reactivity (glial fibrillary acid protein-immunostaining), myelin (myelin basic protein immunoreactivity), ultrastructure, and brain derived neurotrophic factor (BDNF) levels were assessed in non-diabetic and diabetic animals housed in SE or EE. No differences in retinal morphology or retinal ganglion cell number were observed among groups. EE housing which did not affect the STZ-induced weight loss and hyperglycemia, prevented a decrease in the anterograde transport from the retina to the superior colliculus, ON axon number, and phosphorylated neurofilament heavy immunoreactivity. Moreover, EE housing prevented an increase in Iba-1 immunoreactivity, and astrocyte reactivity, as well as ultrastructural myelin alterations in the ON distal portion at early stages of diabetes. In addition, EE housing avoided a decrease in BDNF levels induced by experimental diabetes. These results suggest that EE induced neuroprotection in the diabetic visual pathway.

No MeSH data available.


Related in: MedlinePlus

Effect of EE housing on CTB anterograde transport.Photomicrographs showing retinal projections in the superficial layers of the SC from control or diabetic rats housed in SE or EE. Three representative sections (rostral, medial, and caudal) for each group are shown. In SE-housed animals that were diabetic for 6 weeks, a clear reduction in the density of retinal terminals and zones of no CTB staining were found, particularly in the lateral area. EE housing which was ineffective in non-diabetic animals, preserved CTB anterograde transport in diabetic animals. Dorsal views of a retinotopic SC map reconstruction, representative of 6 animals per group are also shown. Scale bar = 1 mm.
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pone.0136637.g001: Effect of EE housing on CTB anterograde transport.Photomicrographs showing retinal projections in the superficial layers of the SC from control or diabetic rats housed in SE or EE. Three representative sections (rostral, medial, and caudal) for each group are shown. In SE-housed animals that were diabetic for 6 weeks, a clear reduction in the density of retinal terminals and zones of no CTB staining were found, particularly in the lateral area. EE housing which was ineffective in non-diabetic animals, preserved CTB anterograde transport in diabetic animals. Dorsal views of a retinotopic SC map reconstruction, representative of 6 animals per group are also shown. Scale bar = 1 mm.

Mentions: The average body weight and glycemia of SE- or EE-housed animals at 6 weeks after the injection of vehicle or STZ are shown in Table 1. A significant weight loss and an increase in blood glucose levels were observed in STZ-treated rats, as compared with vehicle-injected rats. EE housing did not change these parameters in control or diabetic animals. The active anterograde transport from retinal ganglion cells (RGCs) to the SC at 6 weeks of diabetes induction was analyzed using CTB. In rodents, virtually all RGCs project to the stratum zonale and the stratum griseum superficiale of the contralateral SC. In non-diabetic animals, intensely CTB-stained retinal terminals were observed in the SC (Fig 1). After 6 weeks of diabetes onset, a clear reduction in CTB-staining was observed in the SC from animals housed in SE, whereas in EE-housed diabetic animals, the deficit in CTB transport induced by experimental diabetes was prevented (Fig 1). EE housing did not affect CTB anterograde transport in non-diabetic animals.


Enriched Environment Protects the Optic Nerve from Early Diabetes-Induced Damage in Adult Rats.

Dorfman D, Aranda ML, Rosenstein RE - PLoS ONE (2015)

Effect of EE housing on CTB anterograde transport.Photomicrographs showing retinal projections in the superficial layers of the SC from control or diabetic rats housed in SE or EE. Three representative sections (rostral, medial, and caudal) for each group are shown. In SE-housed animals that were diabetic for 6 weeks, a clear reduction in the density of retinal terminals and zones of no CTB staining were found, particularly in the lateral area. EE housing which was ineffective in non-diabetic animals, preserved CTB anterograde transport in diabetic animals. Dorsal views of a retinotopic SC map reconstruction, representative of 6 animals per group are also shown. Scale bar = 1 mm.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4552300&req=5

pone.0136637.g001: Effect of EE housing on CTB anterograde transport.Photomicrographs showing retinal projections in the superficial layers of the SC from control or diabetic rats housed in SE or EE. Three representative sections (rostral, medial, and caudal) for each group are shown. In SE-housed animals that were diabetic for 6 weeks, a clear reduction in the density of retinal terminals and zones of no CTB staining were found, particularly in the lateral area. EE housing which was ineffective in non-diabetic animals, preserved CTB anterograde transport in diabetic animals. Dorsal views of a retinotopic SC map reconstruction, representative of 6 animals per group are also shown. Scale bar = 1 mm.
Mentions: The average body weight and glycemia of SE- or EE-housed animals at 6 weeks after the injection of vehicle or STZ are shown in Table 1. A significant weight loss and an increase in blood glucose levels were observed in STZ-treated rats, as compared with vehicle-injected rats. EE housing did not change these parameters in control or diabetic animals. The active anterograde transport from retinal ganglion cells (RGCs) to the SC at 6 weeks of diabetes induction was analyzed using CTB. In rodents, virtually all RGCs project to the stratum zonale and the stratum griseum superficiale of the contralateral SC. In non-diabetic animals, intensely CTB-stained retinal terminals were observed in the SC (Fig 1). After 6 weeks of diabetes onset, a clear reduction in CTB-staining was observed in the SC from animals housed in SE, whereas in EE-housed diabetic animals, the deficit in CTB transport induced by experimental diabetes was prevented (Fig 1). EE housing did not affect CTB anterograde transport in non-diabetic animals.

Bottom Line: Diabetic retinopathy is a leading cause of reduced visual acuity and acquired blindness.EE housing which did not affect the STZ-induced weight loss and hyperglycemia, prevented a decrease in the anterograde transport from the retina to the superior colliculus, ON axon number, and phosphorylated neurofilament heavy immunoreactivity.These results suggest that EE induced neuroprotection in the diabetic visual pathway.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Retinal Neurochemistry and Experimental Ophthalmology, Department of Human Biochemistry, School of Medicine/CEFyBO, University of Buenos Aires/CONICET, Buenos Aires, Argentina.

ABSTRACT
Diabetic retinopathy is a leading cause of reduced visual acuity and acquired blindness. Axoglial alterations of the distal (close to the chiasm) optic nerve (ON) could be the first structural change of the visual pathway in streptozotocin (STZ)-induced diabetes in rats. We analyzed the effect of environmental enrichment on axoglial alterations of the ON provoked by experimental diabetes. For this purpose, three days after vehicle or STZ injection, animals were housed in enriched environment (EE) or remained in a standard environment (SE) for 6 weeks. Anterograde transport, retinal morphology, optic nerve axons (toluidine blue staining and phosphorylated neurofilament heavy immunoreactivity), microglia/macrophages (ionized calcium binding adaptor molecule 1 (Iba-1) immunoreactivity), astrocyte reactivity (glial fibrillary acid protein-immunostaining), myelin (myelin basic protein immunoreactivity), ultrastructure, and brain derived neurotrophic factor (BDNF) levels were assessed in non-diabetic and diabetic animals housed in SE or EE. No differences in retinal morphology or retinal ganglion cell number were observed among groups. EE housing which did not affect the STZ-induced weight loss and hyperglycemia, prevented a decrease in the anterograde transport from the retina to the superior colliculus, ON axon number, and phosphorylated neurofilament heavy immunoreactivity. Moreover, EE housing prevented an increase in Iba-1 immunoreactivity, and astrocyte reactivity, as well as ultrastructural myelin alterations in the ON distal portion at early stages of diabetes. In addition, EE housing avoided a decrease in BDNF levels induced by experimental diabetes. These results suggest that EE induced neuroprotection in the diabetic visual pathway.

No MeSH data available.


Related in: MedlinePlus