Increase of extracellular insulin-like growth factor I (IGF-I) concentration following electrolytical lesion in rat hippocampus

Yamaguchi, Fuminori; Itano, Toshifumi; Miyamoto, Osamu; Janjua, Najma A.; Ohmoto, Takashi; Hosokawa, Kiyoshi; Hatase, Osamu

doi:10.1016/0304-3940(91)90278-2

Cited by 44 publications

(14 citation statements)

References 20 publications

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“…Similar findings have been reported by several laboratories in immature [7,13] and adult [14] rats. In addition to changes after acute brain injury, plasma concentrations of IGF-1 decline with aging and IGF-1 deficiency is closely related to the onset and progress of agerelated neurodegenerative conditions [15].…”

Section: Endogenous Response Of Igf-1 To Brain Injurysupporting

confidence: 90%

The role for IGF-1-derived small neuropeptides as a therapeutic target for neurological disorders

Guan

Harris

Brimble

et al. 2015

Expert Opinion on Therapeutic Targets

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These small neuropeptides provide effective neuroprotection by offering an improved pharmacokinetic profile and more practical route of administration compared with IGF-1 administration. Developing modified neuropeptides to overcome the limitations of their endogenous counterparts represents a novel strategy of pharmaceutical discovery for neurological disorders. The mechanism of action may involve a regulation of IGF-1 bioavailability.

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Section: Endogenous Response Of Igf-1 To Brain Injurysupporting

confidence: 90%

The role for IGF-1-derived small neuropeptides as a therapeutic target for neurological disorders

Guan

Harris

Brimble

et al. 2015

Expert Opinion on Therapeutic Targets

View full text Add to dashboard Cite

show abstract

“…Similar findings have also been reported by Lee and Bondy in immature (Lee et al. , 1993; 1996) and adult (Yamaguchi et al. , 1991) rats.…”

Section: Introductionsupporting

confidence: 91%

IGF‐1 derived small neuropeptides and analogues: a novel strategy for the development of pharmaceuticals for neurological conditions

Guan

Gluckman

2009

British J Pharmacology

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Insulin-like growth factor-1 (IGF-1) is neuroprotective and improves long-term function after brain injury. However, its clinical application to neurological disorders is limited by its large molecular size, poor central uptake and mitogenic potential. Glycine-proline-glutamate (GPE) is naturally cleaved from the IGF-1 N-terminal and it is also neuroprotective after ischemic injury, which provided a novel strategy of drug discovery for neurological disorders. GPE is not enzymatically stable, thus intravenous infusion of GPE becomes necessary for stable and potent neuroprotection. The broad effective dose range and treatment window of 3-7 h after the lesion suggest its potential for treating acute brain injuries. G-2meth-PE, a GPE analogue designed to be more enzymatic resistant, has a prolonged plasma half-life and is more potent in neuroprotection. Neuroprotection by GPE and its analogue may involve modulation of inflammation, promotion of astrocytosis, inhibition of apoptosis and vascular remodelling. Acute administration of GPE also prevents 6-OHDA-induced nigrostrial dopamine depletion. Delayed treatment with GPE does not prevent dopamine loss, but improves long-term function. Cyclo-glycyl-proline (cyclic Gly-Pro) is an endogenous DKP that may be derived from GPE. Cyclic Gly-Pro and its analogue cyclo-L-glycyl-L-2-allylproline (NNZ 2591) are both neuroprotective after ischaemic injury. NNZ2591 is highly enzymatic resistant and centrally accessible. Its peripheral administration improves somatosensory-motor function and long-term histological outcome after brain injury. Our research suggests that small neuropeptides have advantages over growth factors in the treatment of brain injury, and that modified neuropeptides designed to overcome the limitations of their endogenous counterparts represent a novel strategy of pharmaceutical discovery for neurological disorders.

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“…Although increases in IGF-1 mRNA or immunoreactivity have been reported to accompany other types of CNS lesions (Yamaguchi et al, 1991;Garcia-Estrada et al, 1992;Komoly et al, 1992;Lee et al, 1992), ours is the first direct demonstration of expression by microglia. With experimentally induced demyelination (Komoly et al, 1992) and transient forebrain ischemia (Lee et al, 19921, IGF-1 expression has been localized to GFAP-positive astrocytes.…”

Section: Discussionmentioning

confidence: 66%

Insulin‐like growth factor‐1 mRNA is increased in deafferented hippocampus: Spatiotemporal correspondence of a trophic event with axon sprouting

Guthrie

Nguyen

Gall

1995

J of Comparative Neurology

111

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Deafferentation is known to induce axonal sprouting in adult brain, but the signals that direct this response are not understood. To evaluate the possible roles of insulin-like growth factor-1 (IGF-1) and basic fibroblast growth factor (bFGF) in central axonal sprouting, the present study used in situ hybridization to evaluate IGF-1 and bFGF mRNA expression in entorhinal deafferented rat hippocampus. Alternate tissue sections were processed for Fink-Heimer impregnation of axonal degeneration, Bandeiraea simplicifolia (BS-1) labeling of microglia, and glial fibrillary acidic protein immunocytochemistry. In control hippocampus, IGF-1 mRNA was localized to a few neurons, with no labeled cells in the dentate gyrus molecular layer; bFGF cRNA hybridization was diffuse in dendritic fields but was dense in CA2 stratum pyramidale. Both mRNA species were increased by deafferentation. The distribution of elevated IGF-1 mRNA corresponded precisely to fields of axonal degeneration and was greatest in the dentate gyrus outer molecular layer and stratum lacunosum moleculare. In these fields, IGF-1 mRNA was elevated by 2 days, reached maximal levels at 4 days, and declined by 10 days postlesion. Double labeling revealed that the majority of IGF-1 cRNA-labeled cells were microglia. In deafferented hippocampus, bFGF mRNA was broadly increased across fields both containing and lacking axonal degeneration. In the dentate, bFGF mRNA levels peaked at 5 days postlesion and remained elevated through 14 days. These results demonstrate that reactive microglia within deafferented hippocampal laminae express IGF-1 mRNA just prior to and during the period of reactive axonal growth and suggest that IGF-1 plays a role in directing the sprouting of spared afferents into these fields.

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Increase of extracellular insulin-like growth factor I (IGF-I) concentration following electrolytical lesion in rat hippocampus

Cited by 44 publications

References 20 publications

The role for IGF-1-derived small neuropeptides as a therapeutic target for neurological disorders

The role for IGF-1-derived small neuropeptides as a therapeutic target for neurological disorders

IGF‐1 derived small neuropeptides and analogues: a novel strategy for the development of pharmaceuticals for neurological conditions

Insulin‐like growth factor‐1 mRNA is increased in deafferented hippocampus: Spatiotemporal correspondence of a trophic event with axon sprouting

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