Environmental enrichment restores the reduced expression of cerebellar synaptophysin and the motor coordination impairment in rats prenatally treated with betamethasone

Valencia, Martina; Illanes, Javiera; Santander, Odra; Saavedra, Daniel; Adaros, Melisa; Ibarra, Alice; Saavedra, Gisell; Pascual, Rodrigo

doi:10.1016/j.physbeh.2019.112590

Cited by 8 publications

(14 citation statements)

References 69 publications

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“…It is evident in our findings that animals intoxicated with MeHg, different from the control group, were not able to master the task of walking on the rotating cylinder at fixed speed rotarod protocol indicating motor learning deficit. Furthermore, the number of falls in rotarod is indicative of motor coordination, primarily at fixed speed rotarod protocol [21] , [39] , [80] , [81] , [82] . In our study, the animals MeHg-exposed had a greater number of falls from the rotating bar indicating motor coordination impairment.…”

Section: Discussionmentioning

confidence: 99%

Methylmercury exposure during prenatal and postnatal neurodevelopment promotes oxidative stress associated with motor and cognitive damages in rats: an environmental-experimental toxicology study

et al. 2022

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Section: Discussionmentioning

confidence: 99%

Methylmercury exposure during prenatal and postnatal neurodevelopment promotes oxidative stress associated with motor and cognitive damages in rats: an environmental-experimental toxicology study

et al. 2022

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“…Early studies in rodents indicate that EE increases total brain and cortical weight [71]. Subsequent studies document additional benefits of EE including increased neuronal density [72], dendritic branching [73] and neuronal transmission [74], and enhanced neurotrophic growth factor expression [75]. EE-induced hormonal and neurostructural changes are also associated with improvements of neural function [76.77].…”

Section: Discussionmentioning

confidence: 99%

Environmental Enrichment Protects Against Cognition Deficits Caused by Sepsis-Associated Encephalopathy

Jiang

Zhao

Tang

et al. 2021

Preprint

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Background: Sepsis-associated encephalopathy (SAE) is a common complication of sepsis and characterized by impaired cognition ability in survivors. Previous studies revealed that environmental enrichment (EE) ameliorated the cognition deficits in different models of brain injury. However, little research exists exploring the effect of EE on SAE. Methods: our present study was designed to determine the possible benefits of EE in ameliorating the cognition deficits following SAE. To examine the benefits of EE, adult male rats with SAE were placed in an enriched environment or standard environment(SE) for 30 days. After the EE or SE housing, the rats were subjected to a behavioral test battery including sensory neglect test (SN), Elevated Plus Maze test (EPM), Open Field test (OF) Morris water maze test (MWM), and Novel Object Recognition test (NOR). Results: Our results showed that SAE-induced the impairment of recognition memory (NOR) and spatial learning and memory (MWM) was significantly inhibited in EE exposed rats. In addition, EE exposure also decreased the SAE-induced anxiety-like behavior (EPM) and increased exploratory activity (OF). However, no difference in locomotion ability was detected between the EE and SE exposed rats. Conclusions: Our results demonstrate the positive effect of EE on cognitive impairments after SAE. These results highlight the importance of environmental enrichment to prevent cognitive deficits induced by SAE.

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“…In contrast to GAD, the amount of VGAT in PC12 cells was maintained in dexamethasone-stimulated PC12 cells. Gephrin with an apparent molecular weight of 98 KDa [50], one of the proteins anchoring GABA A Rs to the subsynaptic membrane in the brain [51][52], was detected in the non-stimulated PC12 homogenates. However, NGF stimulation abolished the expression of gephrin in PC12 cells, and the expression level of gephrin in PC12 cells was not maintained by dexamethasone stimulation.…”

Section: Proteins Involved In Gaba Signalingmentioning

confidence: 99%

Nerve growth factor- and non-stimulated PC12 cells as models for sympathetic ganglion neurons and adrenal chromaffin cells

Harada

Matsuoka

Inoue

2022

Preprint

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PC12 cells are an immortalized cell line originating from rat adrenal medullary chromaffin (AMC) cells and extend a neurite-like structure in response to nerve growth factor (NGF). Thus, non-stimulated and NGF-stimulated PC12 cells are used as model cells for AMC cells and sympathetic ganglion cells, respectively. However, how closely non-stimulated and stimulated PC12 cells resemble AMC cells and sympathetic neurons, respectively, has not sufficiently been elucidated. In addition, how the properties of PC12 cells are affected by NGF remains unclear. These issues were explored by using biochemical and immunocytochemical methods. AMC cells and PC12 cells selectively expressed UCP3 and UCP4, respectively, key proteins which are involved in energy metabolism in a cell-specific manner, and glucocorticoid activity exerted an inhibitory effect on UCP4 expression in PC12 cells. The expression levels of chromaffin granule-associated proteins in PC12 cells were extremely small, whereas the amount of synaptophysin, a synaptic vesicle-associated protein, was much larger than that in the adrenal medulla. As found in AMC cells, the muscarinic receptor subtype 1 (M1R) were located at the cell periphery in basal PC12 cells, as was markedly enhanced by NGF. Furthermore, the proteins involved in GABA auto/paracrine function in AMC cells were expressed in non-stimulated PC12 cells, but not in NGF-stimulated cells. The results suggest that the properties of basal PC12 cells are between those of AMC cells and sympathetic ganglion cells, and glucocorticoid activity and NGF induce differentiation into AMC cells and sympathetic neurons, respectively, and GABA functions as an auto/paracrine factor in AMC cells.

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Environmental enrichment restores the reduced expression of cerebellar synaptophysin and the motor coordination impairment in rats prenatally treated with betamethasone

Cited by 8 publications

References 69 publications

Methylmercury exposure during prenatal and postnatal neurodevelopment promotes oxidative stress associated with motor and cognitive damages in rats: an environmental-experimental toxicology study

Methylmercury exposure during prenatal and postnatal neurodevelopment promotes oxidative stress associated with motor and cognitive damages in rats: an environmental-experimental toxicology study

Environmental Enrichment Protects Against Cognition Deficits Caused by Sepsis-Associated Encephalopathy

Nerve growth factor- and non-stimulated PC12 cells as models for sympathetic ganglion neurons and adrenal chromaffin cells

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