Insulin-like growth factor-I enhances the biological activity of brain-derived neurotrophic factor on cerebrocortical neurons

Robert H. McCusker; Katherine McCrea; Samantha Zunich; Robert Dantzer; Suzanne R. Broussard; Rodney W. Johnson; Keith W. Kelley

doi:10.1016/j.jneuroim.2006.06.014

Insulin-like growth factor-I enhances the biological activity of brain-derived neurotrophic factor on cerebrocortical neurons

Robert H. McCusker, Katherine McCrea, Samantha Zunich, Robert Dantzer, Suzanne R. Broussard, Rodney W. Johnson, Keith W. Kelley

Research output: Contribution to journal › Article › peer-review

Abstract

Insulin-like growth factor (IGF)-I and brain-derived neurotrophic factor (BDNF) act within the brain to enhance neuronal survival and plasticity. We extend these findings by showing that the presence of both neurotrophins is required to depress the rise in intracellular Ca²⁺ caused by glutamate in primary cultures of cerebrocortical neurons. IGF-I enhanced expression of BDNF receptors (Trk-B) and increased the ability of BDNF to induce ERK1/2 phosphorylation. This IGF-I-induced increase in BDNF responsiveness describes a new interaction between these peptides in the brain.

Original language	English (US)
Pages (from-to)	186-190
Number of pages	5
Journal	Journal of Neuroimmunology
Volume	179
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2006.06.014
State	Published - Oct 2006
Externally published	Yes

Keywords

Calcium
ERK
MAPK
Trk-B

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Neurology
Clinical Neurology

Online availability

10.1016/j.jneuroim.2006.06.014

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title = "Insulin-like growth factor-I enhances the biological activity of brain-derived neurotrophic factor on cerebrocortical neurons",

abstract = "Insulin-like growth factor (IGF)-I and brain-derived neurotrophic factor (BDNF) act within the brain to enhance neuronal survival and plasticity. We extend these findings by showing that the presence of both neurotrophins is required to depress the rise in intracellular Ca2+ caused by glutamate in primary cultures of cerebrocortical neurons. IGF-I enhanced expression of BDNF receptors (Trk-B) and increased the ability of BDNF to induce ERK1/2 phosphorylation. This IGF-I-induced increase in BDNF responsiveness describes a new interaction between these peptides in the brain.",

keywords = "Calcium, ERK, MAPK, Trk-B",

author = "McCusker, {Robert H.} and Katherine McCrea and Samantha Zunich and Robert Dantzer and Broussard, {Suzanne R.} and Johnson, {Rodney W.} and Kelley, {Keith W.}",

note = "Funding Information: Supported by the NIH to KWK (MH 51569), RWJ (AG023580) and RD (MH71349) and the USDA to RHM (AG 2004-35206-14144).",

year = "2006",

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doi = "10.1016/j.jneuroim.2006.06.014",

language = "English (US)",

volume = "179",

pages = "186--190",

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AU - McCusker, Robert H.

AU - McCrea, Katherine

AU - Zunich, Samantha

AU - Dantzer, Robert

AU - Broussard, Suzanne R.

AU - Johnson, Rodney W.

AU - Kelley, Keith W.

N1 - Funding Information: Supported by the NIH to KWK (MH 51569), RWJ (AG023580) and RD (MH71349) and the USDA to RHM (AG 2004-35206-14144).

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Y1 - 2006/10

N2 - Insulin-like growth factor (IGF)-I and brain-derived neurotrophic factor (BDNF) act within the brain to enhance neuronal survival and plasticity. We extend these findings by showing that the presence of both neurotrophins is required to depress the rise in intracellular Ca2+ caused by glutamate in primary cultures of cerebrocortical neurons. IGF-I enhanced expression of BDNF receptors (Trk-B) and increased the ability of BDNF to induce ERK1/2 phosphorylation. This IGF-I-induced increase in BDNF responsiveness describes a new interaction between these peptides in the brain.

AB - Insulin-like growth factor (IGF)-I and brain-derived neurotrophic factor (BDNF) act within the brain to enhance neuronal survival and plasticity. We extend these findings by showing that the presence of both neurotrophins is required to depress the rise in intracellular Ca2+ caused by glutamate in primary cultures of cerebrocortical neurons. IGF-I enhanced expression of BDNF receptors (Trk-B) and increased the ability of BDNF to induce ERK1/2 phosphorylation. This IGF-I-induced increase in BDNF responsiveness describes a new interaction between these peptides in the brain.

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KW - ERK

KW - MAPK

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Insulin-like growth factor-I enhances the biological activity of brain-derived neurotrophic factor on cerebrocortical neurons

Abstract

Keywords

ASJC Scopus subject areas

Online availability

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