PUBLICATION
Hyperglycemia induces memory impairment linked to increased acetylcholinesterase activity in zebrafish (Danio rerio)
- Authors
- Capiotti, K.M., Moraes, D.A., Menezes, F.P., Kist, L.W., Bogo, M.R., Silva, R.S.
- ID
- ZDB-PUB-140827-4
- Date
- 2014
- Source
- Behavioural brain research 274: 319-25 (Journal)
- Registered Authors
- Keywords
- Cholinergic system, Diabetes mellitus, Glucose, Hyperglycemia, Locomotor activity., Memory
- MeSH Terms
-
- Acetylcholinesterase/genetics
- Acetylcholinesterase/metabolism*
- Analysis of Variance
- Animals
- Avoidance Learning/drug effects
- Brain/drug effects
- Brain/enzymology*
- Cholinesterase Inhibitors/therapeutic use
- Disease Models, Animal
- Escape Reaction/drug effects
- Female
- Galantamine/therapeutic use
- Gene Expression Regulation/drug effects
- Glucose/toxicity
- Glucose Transporter Type 3/genetics
- Glucose Transporter Type 3/metabolism
- Hyperglycemia/chemically induced
- Hyperglycemia/complications*
- Male
- Memory Disorders/drug therapy
- Memory Disorders/enzymology*
- Memory Disorders/etiology*
- Memory Disorders/pathology
- Motor Activity/drug effects
- Receptor, Insulin/genetics
- Receptor, Insulin/metabolism
- Zebrafish
- PubMed
- 25157430 Full text @ Behav. Brain Res.
Citation
Capiotti, K.M., Moraes, D.A., Menezes, F.P., Kist, L.W., Bogo, M.R., Silva, R.S. (2014) Hyperglycemia induces memory impairment linked to increased acetylcholinesterase activity in zebrafish (Danio rerio). Behavioural brain research. 274:319-25.
Abstract
Diabetes mellitus, which causes hyperglycemia, affects the central nervous system and can impairs cognitive functions, such as memory. The aim of this study was to investigate the effects of hyperglycemia on memory as well as on the activity of acethylcholinesterase. Hyperglycemia was induced in adult zebrafish by immersion in glucose 111mM by 14 days. The animals were divided in 4 groups: control, glucose-treated, glucose-washout 7-days and glucose-washout 14-days. We evaluated the performance in inhibitory avoidance task and locomotor activity. We also determined acethylcholinesterase activity and gene expression from whole brain. In order to counteract the effect of hyperglycemia underlined by effects on acethylcholinesterase activity, we treated the animals with galantamine (0.05ng/g), an inhibitor of this enzyme. Also we evaluated the gene expression of insulin receptor and glucose transporter from zebrafish brain. The hyperglycemia promoted memory deficit in adult zebrafish, which can be explained by increased AChE activity. The ache mRNA levels from zebrafish brain were decrease in 111mM glucose group and returned to normal levels after 7 days of glucose withdrawal. Insulin receptors (insra-1, insra-2, insrb-1 and insrb-2) and glut-3 mRNA levels were not significantly changed. Our results also demonstrated that galantamine was able to reverse the memory deficit caused by hyperglycemia, demonstrating that these effects involve modulation of AChE activity. These data suggest that the memory impairment induced by hyperglycemia is underlined by the cholinergic dysfunction caused by the mechanisms involving the control of acetylcholinesterase function and gene expression.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping