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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

Retinal histology and RGC analysis.Panel A: Representative photomicrographs showing the histologic appearance of retinas from control or diabetic rats housed in SE or EE for 6 weeks (hematoxylin and eosin staining). No obvious differences in the retinal structure were observed among groups. OS, photoreceptor outer segments; INL, inner nuclear layer; IPL, inner plexiform layer; ONL, outer nuclear layer; OPL, outer plexiform layer; GCL, ganglion cell layer. Panel B: Shown are representative photomicrographs of Brn3a immunostaining in flat-mounted retinas in center and periphery from 5 animals/group. Scale bar: 50 μm.
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pone.0136637.g002: Retinal histology and RGC analysis.Panel A: Representative photomicrographs showing the histologic appearance of retinas from control or diabetic rats housed in SE or EE for 6 weeks (hematoxylin and eosin staining). No obvious differences in the retinal structure were observed among groups. OS, photoreceptor outer segments; INL, inner nuclear layer; IPL, inner plexiform layer; ONL, outer nuclear layer; OPL, outer plexiform layer; GCL, ganglion cell layer. Panel B: Shown are representative photomicrographs of Brn3a immunostaining in flat-mounted retinas in center and periphery from 5 animals/group. Scale bar: 50 μm.

Mentions: At 6 weeks after vehicle or STZ injection, Brn3a-immunoreactivity in the central and peripheral retina did not differ among groups, as shown in Fig 2. In addition, no differences in the total retinal thickness, GCL cell number, and Brn3a(+) cell number were observed among groups (Table 2). EE housing did not affect these parameters in non-diabetic rats.


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

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

Retinal histology and RGC analysis.Panel A: Representative photomicrographs showing the histologic appearance of retinas from control or diabetic rats housed in SE or EE for 6 weeks (hematoxylin and eosin staining). No obvious differences in the retinal structure were observed among groups. OS, photoreceptor outer segments; INL, inner nuclear layer; IPL, inner plexiform layer; ONL, outer nuclear layer; OPL, outer plexiform layer; GCL, ganglion cell layer. Panel B: Shown are representative photomicrographs of Brn3a immunostaining in flat-mounted retinas in center and periphery from 5 animals/group. Scale bar: 50 μm.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0136637.g002: Retinal histology and RGC analysis.Panel A: Representative photomicrographs showing the histologic appearance of retinas from control or diabetic rats housed in SE or EE for 6 weeks (hematoxylin and eosin staining). No obvious differences in the retinal structure were observed among groups. OS, photoreceptor outer segments; INL, inner nuclear layer; IPL, inner plexiform layer; ONL, outer nuclear layer; OPL, outer plexiform layer; GCL, ganglion cell layer. Panel B: Shown are representative photomicrographs of Brn3a immunostaining in flat-mounted retinas in center and periphery from 5 animals/group. Scale bar: 50 μm.
Mentions: At 6 weeks after vehicle or STZ injection, Brn3a-immunoreactivity in the central and peripheral retina did not differ among groups, as shown in Fig 2. In addition, no differences in the total retinal thickness, GCL cell number, and Brn3a(+) cell number were observed among groups (Table 2). EE housing did not affect these parameters in non-diabetic rats.

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