Hyperglycemia induces memory impairment linked to increased acetylcholinesterase activity in zebrafish (Danio rerio)

Capiotti, Katiúcia Marques; Moraes, Daiani Almeida De; Menezes, Fabiano Peres; Kist, Luiza Wilges; Bogo, Maurı́cio Reis; Silva, Rosane Souza da

doi:10.1016/j.bbr.2014.08.033

Cited by 68 publications

(40 citation statements)

References 49 publications

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“…After, we performed the evaluation of the E-NTPDases, ada-related, and adora gene expressions from encephala of adult zebrafish. The blood glucose levels from glucose-treated and washout animals demonstrated the same profile already developed in previous works [8,42]. Nucleotides are important extracellular messengers in both physiological and pathological conditions [11].…”

Section: Discussionsupporting

confidence: 75%

Hyperglycemia alters E-NTPDases, ecto-5′-nucleotidase, and ectosolic and cytosolic adenosine deaminase activities and expression from encephala of adult zebrafish (Danio rerio)

Capiotti

Siebel

Kist

et al. 2016

Purinergic Signalling

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Hyperglycemia is the main feature for the diagnosis of diabetes mellitus (DM). Some studies have demonstrated the relationship between DM and dysfunction on neurotransmission systems, such as the purinergic system. In this study, we evaluated the extracellular nucleotide hydrolysis and adenosine deamination activities from encephalic membranes of hyperglycemic zebrafish. A significant decrease in ATP, ADP, and AMP hydrolyses was observed at 111-mM glucose-treated group, which returned to normal levels after 7 days of glucose withdrawal. A significant increase in ectoadenosine deaminase activity was observed in 111-mM glucose group, which remain elevated after 7 days of glucose withdrawal. The soluble-adenosine deaminase activity was significantly increased just after 7 days of glucose withdrawal. We also evaluated the gene expressions of ecto-nucleoside triphosphate diphosphohydrolases (E-NTPDases), ecto-5′-nucleotidase, ADA, and adenosine receptors from encephala of adult zebrafish. The entpd 2a.1, entpd 2a.2, entpd 3, and entpd 8 mRNA levels from encephala of adult zebrafish were decreased in 111-mM glucose-treated and glucose withdrawal groups. The gene expressions of adenosine receptors (adora 1 , adora 2aa , adora 2ab , and adora 2b ) were decreased in 111-mM glucose-treated and glucose withdrawal groups. The gene expression of ADA (ada 2a.1) was decreased in glucose withdrawal group. Maltodextrin, used as a control, did not affect the expression of adenosine receptors, ADA and E-NTPDases 2, 3, and 8, while the expression of ecto-5′-nucleotidase was slightly increased and the E-NTPDases 1 decreased. These findings demonstrated that hyperglycemia might affect the ecto-nucleotidase and adenosine deaminase activities and gene expression in zebrafish, probably through a mechanism involving the osmotic effect, suggesting that the modifications caused on purinergic system may also contribute to the diabetes-induced progressive cognitive impairment.

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Section: Discussionsupporting

confidence: 75%

Hyperglycemia alters E-NTPDases, ecto-5′-nucleotidase, and ectosolic and cytosolic adenosine deaminase activities and expression from encephala of adult zebrafish (Danio rerio)

Capiotti

Siebel

Kist

et al. 2016

Purinergic Signalling

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“…47 Acetylcholinesterase, a surrogate marker of dementia, is increased after menopause and diabetes. 46,48 We also observed a significant increase in acetylcholinesterase activity (58.2%) in Ovx-Dia rats compared with their respective controls. A selective ER-b agonist more markedly reduced (52.5%) this activity toward reference levels in Ovx-Dia rats than did E 2 (40.2%) and an ER-a agonist (21.1%).…”

Section: Er Agonists In Postmenopausal Diabetesmentioning

confidence: 65%

Differential role of estrogen receptor modulators in depression-like behavior and memory impairment in rats with postmenopausal diabetes

Bansal

Chopra

2015

Menopause

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“…It is interesting to note that diabetes is also known for impairing brain memory (Whitmer, 2007;Ho et al, 2013). Recently, using the same experimental conditions, Capiotti and colleagues demonstrated that hyperglycemia induces memory impairment in adult zebrafish (Capiotti et al, 2014b), similar to the mammalian situation. Taken together, these data demonstrate that hyperglycemia in zebrafish impairs brain functions such as neurogenesis and memory.…”

Section: Neurogenesismentioning

confidence: 94%

Impaired constitutive and regenerative neurogenesis in adult hyperglycemic zebrafish

Dorsemans

Soulé

Weger

et al. 2016

J of Comparative Neurology

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A growing body of evidence supports hyperglycemia as a putative contributor to several brain dysfunctions observed in diabetes patients, such as impaired memory capacity, neural plasticity, and neurogenic processes. Thanks to the persistence of radial glial cells acting as neural stem cells, the brain of the adult zebrafish constitutes a relevant model to investigate constitutive and injury-induced neurogenesis in adult vertebrates. However, there is limited understanding of the impact of hyperglycemia on brain dysfunction in the zebrafish model. This work aimed at exploring the impact of acute and chronic hyperglycemia on brain homeostasis and neurogenesis. Acute hyperglycemia was shown to promote gene expression of proinflammatory cytokines (il1β, il6, il8, and tnfα) in the brain and chronic hyperglycemia to impair expression of genes involved in the establishment of the blood-brain barrier (claudin 5a, zona occludens 1a and b). Chronic hyperglycemia also decreased brain cell proliferation in most neurogenic niches throughout the forebrain and the midbrain. By using a stab wound telencephalic injury model, the impact of hyperglycemia on brain repair mechanisms was investigated. Whereas the initial step of parenchymal cell proliferation was not affected by acute hyperglycemia, later proliferation of neural progenitors was significantly decreased by chronic hyperglycemia in the injured brain of fish. Taken together, these data offer new evidence highlighting the evolutionary conserved adverse effects of hyperglycemia on neurogenesis and brain healing in zebrafish. In addition, our study reinforces the utility of zebrafish as a robust model for studying the effects of metabolic disorders on the central nervous system. J. Comp. Neurol. 525:442-458, 2017. © 2016 Wiley Periodicals, Inc.

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Hyperglycemia induces memory impairment linked to increased acetylcholinesterase activity in zebrafish (Danio rerio)

Cited by 68 publications

References 49 publications

Hyperglycemia alters E-NTPDases, ecto-5′-nucleotidase, and ectosolic and cytosolic adenosine deaminase activities and expression from encephala of adult zebrafish (Danio rerio)

Hyperglycemia alters E-NTPDases, ecto-5′-nucleotidase, and ectosolic and cytosolic adenosine deaminase activities and expression from encephala of adult zebrafish (Danio rerio)

Differential role of estrogen receptor modulators in depression-like behavior and memory impairment in rats with postmenopausal diabetes

Impaired constitutive and regenerative neurogenesis in adult hyperglycemic zebrafish

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