Enriched environment prevents memory deficits in type 1 diabetic rats

Piazza, Francele Valente; Pinto, Guilherme Vanik; Trott, Geraldine; Marcuzzo, Simone; Gomez, Rosane; Fernandes, Marilda da Cruz

doi:10.1016/j.bbr.2010.09.017

Cited by 25 publications

(25 citation statements)

References 31 publications

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“…Interestingly, some previous findings of impaired recognition memory in the STZ model were based on object-placement/spatial-recognition paradigms, rather than on the commonly used object-recognition paradigm employed in the present study [49][50][51]. This methodological difference may explain the lack of any STZ-induced effect in the present study.…”

Section: Discussioncontrasting

confidence: 64%

“…The STZ model has also been used to investigate learning and memory impairments associated with diabetes. STZ treatment is associated with impairments in a variety of cognitive behavioural tasks such as spatial learning in the water maze [12][13][14][15], T-maze active avoidance [16], and object-placement learning tasks [17][18][19]. Learning impairments relate to the duration and severity of diabetes and to the complexity of the cognitive task [20].…”

Section: Introductionmentioning

confidence: 99%

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Impaired cued and spatial learning performance and altered cannabinoid CB1 receptor functionality in the substantia nigra in a rat model of diabetic neuropathy

Moriarty

Lang

Idrees

et al. 2016

Behavioural Brain Research

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Diabetes, and associated diabetic neuropathic pain, impact negatively on cognitive function. However, the underlying mechanisms remain poorly understood. This study investigated neuropathic pain-related behaviour and cognitive function in the rat streptozotocin (STZ) model of diabetes, and assessed cannabinoid1 (CB1) receptor functionality in discrete brain regions. Male Lister-Hooded rats received STZ (60 mg/kgs.c.) or vehicle. Sensory responses were assessed in von Frey and Hargreaves tests. Cognitive, motor and sensorimotor functions were assessed using novel object recognition and Morris water maze tasks. CB1 receptor functionality was assessed by [(35)S]GTPγS (guanosine 5'-O-[gamma-thio]triphosphate) autoradiography. STZ treatment was associated with mechanical allodynia and thermal hypoalgesia. Novel object recognition was unaltered in diabetic rats. STZ treatment was associated with impaired performance in the Morris water maze acquisition phase, but there were no differences in memory retrieval in the probe trial. Stimulus-response learning in the water maze cued trial was also disrupted in STZ-treated rats, possibly indicating sensorimotor deficits. CB1 receptor agonist-stimulated [(35)S]GTPγS binding was attenuated in the substantia nigra of STZ-treated rats but unaltered in the hippocampus. In conclusion, STZ treatment as a model of diabetic neuropathy was associated with specific functional deficits in the Morris water maze, effects which may be related to altered CB1 receptor functionality in the substantia nigra.

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Section: Discussioncontrasting

confidence: 64%

Section: Introductionmentioning

confidence: 99%

Impaired cued and spatial learning performance and altered cannabinoid CB1 receptor functionality in the substantia nigra in a rat model of diabetic neuropathy

Moriarty

Lang

Idrees

et al. 2016

Behavioural Brain Research

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“…EE, defined as "modifying the environment of captive animals to enhance their physical and psychological well-being by providing stimuli that meet their specific needs," [15] stimulates hippocampal cell proliferation and survival in rodent models of diabetes. [16,17] Pamidi and Nayak studied this phenomenon in the dual context of stress and diabetes. They subjected rats with streptozotocin-induced diabetes to stress and/or EE and examined hippocampal neurogenesis after 30 days.…”

Section: Spotlight On Original Articlesenvironmental Enrichment Limitmentioning

confidence: 99%

Pointing the finger at proton pump inhibitors

Walton¹

2014

Biomed J

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This issue of the Biomedical Journal welcomes articles from a wide range of disciplines. We take a look at the optimization of surgical techniques in rabbits and visit some of the medical wonders of stem cell technology. In particular, we highlight Sasmita Biswal's discussion of an emerging link between the use of proton pump inhibitors and hospital-acquired Clostridium difficile infections, in addition to intriguing data showing that environmental enrichment protects hippocampal neurons from damage in stressed, diabetic rats. (Biomed J 2014;37:165-168)

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“…Environmental conditions have been shown to rescue the diabetic brain from neurodegenerative progression [9], and to prevent or delay the development of memory deficits caused by diabetes in adult rats [10]. In an enriched environment (EE), animals are allowed the freedom to move and exercise voluntarily in larger cages, with accessibility to complex stimuli (e.g.…”

Section: Introductionmentioning

confidence: 99%

Environmental Enrichment Protects the Retina from Early Diabetic Damage in Adult Rats

et al. 2014

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Diabetic retinopathy is a leading cause of reduced visual acuity and acquired blindness. Available treatments are not completely effective. We analyzed the effect of environmental enrichment on retinal damage induced by experimental diabetes in adult Wistar rats. Diabetes was induced by an intraperitoneal injection of streptozotocin. Three days after vehicle or streptozotocin injection, animals were housed in enriched environment or remained in a standard environment. Retinal function (electroretinogram, and oscillatory potentials), retinal morphology, blood-retinal barrier integrity, synaptophysin, astrocyte and Müller cell glial fibrillary acidic protein, vascular endothelial growth factor, tumor necrosis factor-α, and brain-derived neurotrophic factor levels, as well as lipid peroxidation were assessed in retina from diabetic animals housed in standard or enriched environment. Environmental enrichment preserved scotopic electroretinogram a-wave, b-wave and oscillatory potential amplitude, avoided albumin-Evan's blue leakage, prevented the decrease in retinal synaptophysin and astrocyte glial fibrillary acidic protein levels, the increase in Müller cell glial fibrillary acidic protein, vascular endothelial growth factor and tumor necrosis factor-α levels, as well as oxidative stress induced by diabetes. In addition, enriched environment prevented the decrease in retinal brain-derived neurotrophic factor levels induced by experimental diabetes. When environmental enrichment started 7 weeks after diabetes onset, retinal function was significantly preserved. These results indicate that enriched environment could attenuate the early diabetic damage in the retina from adult rats.

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Enriched environment prevents memory deficits in type 1 diabetic rats

Cited by 25 publications

References 31 publications

Impaired cued and spatial learning performance and altered cannabinoid CB1 receptor functionality in the substantia nigra in a rat model of diabetic neuropathy

Impaired cued and spatial learning performance and altered cannabinoid CB1 receptor functionality in the substantia nigra in a rat model of diabetic neuropathy

Pointing the finger at proton pump inhibitors

Environmental Enrichment Protects the Retina from Early Diabetic Damage in Adult Rats

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