ArticleExperimental brain research2013
Hyperinsulinemia in rats causes impairment of spatial memory and learning with defects in hippocampal synaptic plasticity by involvement of postsynaptic mechanisms.
Article in Experimental brain research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 41 papers.
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41 citing papers in PubMed, 63 citations in OpenAlex.
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- Brain insulin resistance and cognitive function: influence of exercise.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Review
- Diabetes and associated cognitive disorders: Role of the Hypothalamic-Pituitary Adrenal axis.Metabolism open · 2022Review
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Corrections and comments
- Erratum issuedAl Ansari, Amer [removed]
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to its peripheral metabolic functions, insulin acts as a central neuromodulator and affects synaptic plasticity of the hippocampal neurons. In this study, hyperinsulinemic obese zucker rats (OZR) with autosomal recessive mutation of the fa-gene were tested in water maze for learning and memory. The animals were then decapitated and hippocampal slices were prepared for electrophysiological examination. In the water maze test, the OZR performed less efficient than their counter lean control rats (LCR). The OZR showed prolonged latency and increased distance swam to reach a hidden platform. In the electrophysiological experiments, the hippocampal slices were examined for paired-pulse facilitation (PPF), long-term potentiation (LTP), and depression expression. The results showed that while the PPF (thus mainly the presynaptic mechanisms) was not affected, the LTP expression (169.9 ± 16.6 vs. 310.7 ± 2.4 %) and the synaptic plasticity range (69.2 vs. 211.2 %) were both reduced in the OZR animals compared to the LCR. It is concluded that hyperinsulinemia in the OZR resulted in defects in hippocampal synaptic plasticity associated with deterioration in spatial learning and memory functions.
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