Dataset Information

Insulin-like growth factor 1 (IGF-1) mediates the effects of enriched environment (EE) on visual cortical development.

ABSTRACT: Enriched environment (EE) has been recently shown to affect visual cortex development and plasticity, and to prevent dark rearing effects. The factors mediating EE effects on visual cortical development and plasticity are still unclear. We have investigated whether IGF-1 is involved in mediating EE effects on the developing visual cortex. We show that EE increases the number of IGF-1 positive neurons in the visual cortex at P18. Increasing IGF-1 in the visual cortex of non-EE rats by means of osmotic minipumps implanted at P18 mimics EE effects, accelerating visual acuity development, assessed with Visual Evoked Potentials (VEPs). Blocking IGF-1 action in the visual cortex of EE rats by means of the IGF-1 receptor antagonist JB1 from P18 completely blocks EE action on visual acuity development. These results show that IGF-1 is a key factor mediating EE effects on visual cortical development. We then show that IGF-1 affects GAD65 immunoreactivity in perisomatic innervation and the condensation of Chondroitin Sulphate Proteoglycans (CSPGs) in perineuronal nets (PNNs) in the visual cortex. This suggests that IGF-1 action in mediating EE effects could be exerted through the modulation of intracortical inhibitory circuitry and PNN development.

SUBMITTER: Ciucci F

PROVIDER: S-EPMC1871611 | biostudies-literature | 2007 May

REPOSITORIES: biostudies-literature

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Insulin-like growth factor 1 (IGF-1) mediates the effects of enriched environment (EE) on visual cortical development.

Ciucci Francesca F Putignano Elena E Baroncelli Laura L Landi Silvia S Berardi Nicoletta N Maffei Lamberto L

PloS one 20070530 5

Enriched environment (EE) has been recently shown to affect visual cortex development and plasticity, and to prevent dark rearing effects. The factors mediating EE effects on visual cortical development and plasticity are still unclear. We have investigated whether IGF-1 is involved in mediating EE effects on the developing visual cortex. We show that EE increases the number of IGF-1 positive neurons in the visual cortex at P18. Increasing IGF-1 in the visual cortex of non-EE rats by means of os ...[more]

PMID: 17534425

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Project description:Objective. The aim of this review is to explore the role of IGF-1 and IGF-1R inhibitors in pain-related conditions and assess the effectiveness of IGF-1-related drugs in pain management. Specifically, this paper investigates the potential involvement of IGF-1 in nociception, nerve regeneration, and the development of neuropathic pain. Methods. We conducted a search of the PUBMED/MEDLINE database, Scopus, and the Cochrane Library for all reports published in English on IGF-1 in pain management from origination through November 2022. The resulting 545 articles were screened, and 18 articles were found to be relevant after reading abstracts. After further examination of the full text of these articles, ten were included in the analysis and discussion. The levels of clinical evidence and implications for recommendations of all the included human studies were graded. Results. The search yielded 545 articles, of which 316 articles were deemed irrelevant by reading the titles. There were 18 articles deemed relevant after reading abstracts, of which 8 of the reports were excluded due to lack of IGF-1-related drug treatment after reviewing the full text of the articles. All ten articles were retrieved for analysis and discussion. We found that IGF-1 may have several positive effects on pain management, including promoting the resolution of hyperalgesia, preventing chemotherapy-induced neuropathy, reversing neuronal hyperactivity, and elevating the nociceptive threshold. On the other hand, IGF-1R inhibitors may alleviate pain in mice with injury of the sciatic nerve, bone cancer pain, and endometriosis-induced hyperalgesia. While one study showed marked improvement in thyroid-associated ophthalmopathy in humans treated with IGF-1R inhibitor, two other studies did not find any benefits from IGF-1 treatment. Conclusions. This review highlights the potential of IGF-1 and IGF-1R inhibitors in pain management, but further research is needed to fully understand their efficacy and potential side effects.

Project description:Our previous studies showed that Insulin-like Growth Factor (IGF)-1 reduced blood brain barrier permeability and decreased infarct volume caused by middle cerebral artery occlusion (MCAo) in middle aged female rats. Similarly, cultures of primary brain microvessel endothelial cells from middle-aged female rats and exposed to stroke-like conditions (oxygen glucose deprivation; OGD) confirmed that IGF-1 reduced dye transfer across this cell monolayer. Surprisingly, IGF-1 did not attenuate endothelial cell death caused by OGD. To reconcile these findings, the present study tested the hypothesis that, at the earliest phase of ischemia, IGF-1 promotes barrier function by increasing anchorage and stabilizing cell geometry of surviving endothelial cells. Cultures of human brain microvessel endothelial cells were subject to oxygen-glucose deprivation (OGD) in the presence of IGF-1, IGF-1?+?JB-1 (IGFR inhibitor) or vehicle. OGD disrupted the cell monolayer and reduced cell-cell interactions, which was preserved in IGF-1-treated cultures and reversed by concurrent treatment with JB-1. IGF-1-mediated preservation of the endothelial monolayer was reversed with LY294002 treatment, but not by Rapamycin, indicating that IGF-1?s actions on cell-cell contacts are likely mediated via the PI3K pathway. In vivo, microvessel morphology was evaluated in middle-aged female rats that were subjected to ischemia by MCAo, and treated ICV with IGFI, IGF-1?+?JB-1, or artificial CSF (aCSF; vehicle) after reperfusion. Compared to vehicle controls, IGF-1 treated animals displayed larger microvessel diameters in the peri-infarct area and increased staining density for vinculin, an anchorage protein. Both these measures were reversed by concurrent IGF-1?+?JB-1 treatment. Moreover these effects were restricted to 24?h after ischemia-reperfusion and no treatment effects were seen at 5d post stroke. Collectively, these data suggest that in the earliest hours during ischemia, IGF-1 promotes receptor-mediated anchorage of endothelial cells, and its actions may be accurately characterized as vasculoprotective.

Dataset Information

Insulin-like growth factor 1 (IGF-1) mediates the effects of enriched environment (EE) on visual cortical development.

Publications

Insulin-like growth factor 1 (IGF-1) mediates the effects of enriched environment (EE) on visual cortical development.

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