Intracerebroventricular administration of insulin attenuates retrieval of a passive avoidance response in rats

Schwarzberg, H; Bernstein, Hans‐Gert; Reiser, Michael; Günther, Olaf

doi:10.1016/0143-4179(89)90002-4

Cited by 33 publications

(19 citation statements)

References 20 publications

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“…73 The neuroprotective effects of the IR pathway are well documented, 34,74 but it has also been shown that insulin injection could impair brain function. 75,76 Also, a recent paper has reportd findings similar to ours, namely, that insulin injection eliminates the beneficial effects of exercise as shown on the Morris water maze test, and it was suggested that this could be a result of the IR signaling on N-methyl-D-aspartate receptors. 38 Therefore, the available data suggest that activation of IGF-1/insulin signaling could be both beneficial and harmful, thus, stress the importance of the very delicate IR signaling in the brain.…”

supporting

confidence: 52%

Combined Exercise and Insulin-Like Growth Factor-1 Supplementation Induces Neurogenesis in Old Rats, but Do Not Attenuate Age-Associated DNA Damage

Koltai

Zhao

Lacza

et al. 2011

Rejuvenation Research

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We have investigated the effects of 2 weeks of insulin-like growth factor-1 (IGF-1) supplementation (5 mg/kg per day) and 6 weeks of exercise training (60% of the maximal oxygen consumption [VO 2 max]) on neurogenesis, DNA damage/repair, and sirtuin content in the hippocampus of young (3 months old) and old (26 months old) rats. Exercise improved the spatial memory of the old group, but IGF-1 supplementation eliminated this effect. An age-associated decrease in neurogenesis was attenuated by exercise and IGF-1 treatment. Aging increased the levels of 8-oxo-7,8-dihydroguanine (8-oxoG) and the protein Ku70, indicating the role of DNA damage in age-related neuropathology. Acetylation of 8-oxoguanine DNA glycosylase (OGG1) was detected in vivo, and this decreased with aging. However, in young animals, exercise and IGF-1 treatment increased acetylated (ac) OGG1 levels. Sirtuin 1 (SIRT1) and SIRT3, as DNA damage-associated lysine deacetylases, were measured, and SIRT1 decreased with aging, resulting in a large increase in acetylated lysine residues in the hippocampus. On the other hand, SIRT3 increased with aging. Exercise-induced neurogenesis might not be a causative factor of increased spatial memory, because IGF-1 plus exercise can induce neurogenesis in the hippocampus of older rats. Data revealed that the age-associated increase in 8-oxoG levels is due to decreased acetylation of OGG1. Age-associated decreases in SIRT1 and the associated increase in lysine acetylation, in the hippocampus, could have significant impact on function and thus, could suggest a therapeutic target.

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supporting

confidence: 52%

Combined Exercise and Insulin-Like Growth Factor-1 Supplementation Induces Neurogenesis in Old Rats, but Do Not Attenuate Age-Associated DNA Damage

Koltai

Zhao

Lacza

et al. 2011

Rejuvenation Research

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“…Park et al evaluated the effects of ICV administration of insulin on post-training retention of the task in passive avoidance test and have shown that insulin-receiving rats has an increased latency to enter the dark compartment, showing that insulin can enhance the performance of rats in this memory task [162]. In contrast to this report, Schwarzberg et al reported that ICV injection of insulin impairs animal performance in passive avoidance at both 24-and 48-h retention trials [163]. However, it should be noticed that insulin administration in the study of Schwartzberg was prior to the retention trial, whereas in the study of Park, insulin was injected after training trials.…”

Section: Central Insulin Administration and Cognitive Functionmentioning

confidence: 45%

“…According to their view, insulin may have positive effects on memory consolidation but negative affects arousal [162]. Therefore, one explanation for the above-mentioned controversy is that insulin administration prior to training may cause animals to be less alert or attentive and do not perform as well as expected [163]. Another explanation can be the different insulin dosages used in these studies.…”

Section: Central Insulin Administration and Cognitive Functionmentioning

confidence: 88%

Insulin in the Brain: Sources, Localization and Functions

et al. 2012

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Historically, insulin is best known for its role in peripheral glucose homeostasis, and insulin signaling in the brain has received less attention. Insulin-independent brain glucose uptake has been the main reason for considering the brain as an insulin-insensitive organ. However, recent findings showing a high concentration of insulin in brain extracts, and expression of insulin receptors (IRs) in central nervous system tissues have gathered considerable attention over the sources, localization, and functions of insulin in the brain. This review summarizes the current status of knowledge of the peripheral and central sources of insulin in the brain, site-specific expression of IRs, and also neurophysiological functions of insulin including the regulation of food intake, weight control, reproduction, and cognition and memory formation. This review also considers the neuromodulatory and neurotrophic effects of insulin, resulting in proliferation, differentiation, and neurite outgrowth, introducing insulin as an attractive tool for neuroprotection against apoptosis, oxidative stress, beta amyloid toxicity, and brain ischemia.

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“…However, these studies did not test memory retention at later time-points. Furthermore, the conclusion that insulin had an enhancing effect on memory has been controversial: Different doses of insulin and times of administration in relationship to training, as well as systemic administrations, have produced impairing effects on memory (Clayson 1971;Schwarzberg et al 1989;Baratti 1996, 1999;Kopf et al 1998;Moosavi et al 2006). To our knowledge, the only study that reported the effect of insulin on memory persistence was carried out with systemic treatments, and showed memory impairment at 7 and 30 d after training (Kopf and Baratti 1996).…”

Section: Discussionmentioning

confidence: 99%

The effect of insulin and insulin-like growth factors on hippocampus- and amygdala-dependent long-term memory formation

2014

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Recent work has reported that the insulin-like growth factor 2 (IGF2) promotes memory enhancement. Furthermore, impaired insulin or IGF1 functions have been suggested to play a role in the pathogenesis of neurodegeneration and cognitive impairments, hence implicating the insulin/IGF system as an important target for cognitive enhancement and/or the development of novel treatments against cognitive disorders. Here, we tested the effect of intracerebral injections of IGF1, IGF2, or insulin on memory consolidation and persistence in rats. We found that a bilateral injection of insulin into the dorsal hippocampus transiently enhances hippocampal-dependent memory and an injection of IGF1 has no effect. None of the three peptides injected into the amygdala affected memories critically engaging this region. Together with previous data on IGF2, these results indicate that IGF2 produces the most potent and persistent effect as a memory enhancer on hippocampal-dependent memories. We suggest that the memory-enhancing effects of insulin and IGF2 are likely mediated by distinct mechanisms.

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Intracerebroventricular administration of insulin attenuates retrieval of a passive avoidance response in rats

Cited by 33 publications

References 20 publications

Combined Exercise and Insulin-Like Growth Factor-1 Supplementation Induces Neurogenesis in Old Rats, but Do Not Attenuate Age-Associated DNA Damage

Combined Exercise and Insulin-Like Growth Factor-1 Supplementation Induces Neurogenesis in Old Rats, but Do Not Attenuate Age-Associated DNA Damage

Insulin in the Brain: Sources, Localization and Functions

The effect of insulin and insulin-like growth factors on hippocampus- and amygdala-dependent long-term memory formation

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