Enriched environment induces beneficial effects on memory deficits and microglial activation in the hippocampus of type 1 diabetic rats

Abstract

Type 1 diabetes mellitus (T1DM) has been associated with long-term complications in the central nervous system, causing brain cellular dysfunctions and cognitive deficits. On the other hand, enriched environment (EE) induces experience-dependent plasticity, especially in the hippocampus, improving the performance of animals in learning and memory tasks. Thus, our objective was to investigate the influence of the EE on memory deficits, locomotion, corticosterone levels, synaptophysin (SYP) protein immunoreactivity, cell survival and microglial activation in the dentate gyrus (DG) of T1DM rat hippocampus. Male Wistar rats (21-day-old) were exposed to EE or maintained in standard housing (controls, C) for 3 months. At adulthood, the C and EE animals were randomly divided and diabetes was induced in half of them. All the animals received 4 doses of BrdU, 24 h apart. Hippocampus-dependent spatial memory, general locomotion and serum corticosterone levels were evaluated at the end of the experiment. The animals were transcardially perfused 30 days post-BrdU administration. Our results showed that EE was able to prevent/delay the development of memory deficits caused by diabetes in rats, however it did not revert the motor impairment observed in the diabetic group. SYP immunoreactivity was increased in the enriched healthy group. The EE decreased the serum corticosterone levels in diabetic adult rats and attenuated the injurious microglial activation, though without altering the decrease of the survival cell. Thus, EE was shown to help to ameliorate cognitive comorbidities associated with T1DM, possibly by reducing hyperactivity in the hypothalamic-pituitary-adrenal axis and microglial activation in diabetic animals.

Dose‐dependent neurocognitive deficits following postnatal day 10 HIV‐1 viral protein exposure: Relationship to hippocampal anatomy parameters

“…Thus, the results from both studies suggest that spatial learning and/or memory deficits following HIV‐1 viral protein exposure may be due to increased gliosis and/or neuronal loss in the DGH. Previous work has found associations between the DGH and spatial learning and/or memory in multiple disease models, (Zhang et al, 2011; Martinez‐Canabal et al, 2013; Cahill et al, 2014; Piazza et al, 2014; Taylor et al, 2015; Zerwas et al, 2015), supporting the findings of the present study.…”

Enriched Environment Altered Aberrant Hippocampal Neurogenesis and Improved Long-Term Consequences After Temporal Lobe Epilepsy in Adult Rats

“…Considerable evidences had shown that EE treatment was beneficial for cognitive functions both in normal and pathological conditions (Cao et al 2008;Anastasia et al 2009;Hirata et al 2011;Simao et al 2012;Beauquis et al 2013;Doulames et al 2014;Piazza et al 2014). However, few studies addressed whether and how EE Xiaoqian Zhang and Tingting Liu contributed equally to this work.…”

Short‐term exposure to enriched environment rescues chronic stress‐induced impaired hippocampal synaptic plasticity, anxiety, and memory deficits

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