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Issue Cover (December 2019)
Publication year - 2019
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/jnc.14534
Subject(s) - glutamate receptor , insulin like growth factor 1 receptor , insulin like growth factor receptor , receptor , insulin receptor , insulin like growth factor , neuroscience , biology , growth factor , insulin , medicine , endocrinology , insulin resistance
Front cover: Insulin‐like growth factor 1 (IGF‐1) promotes growth and excitability of neurons. The role of IGF‐1 in regulating the function of astrocytes is still not clearly understood. Astrocytes form the major cell type in the brain, and regulate glutamate handling in the brain, thereby protecting neurons and other cells. Our study uses a combination of pharmacological and genetic techniques of manipulating IGFR signaling to examine whether IGF‐1 acts through its cognate receptor IGFR to alter the handling of glutamate by astrocytes in the brain. Our study showed that short‐term inhibition of IGFR resulted in a significant decrease in glutamate transporter availability on the cell surface, thereby decreasing the uptake of glutamate in vitro. Additionally, we saw long‐term inhibition of IGFR resulted in significant reductions in glutamate uptake by decreasing mRNA expression of glutamate transport machinery. Reduced glutamate transporter mRNA was also observed in mice lacking astrocytic IGFR. Together, these data suggest that reduced IGF‐1 signaling will favor an accumulation of extra‐synaptic glutamate, which may contribute to neurodegeneration in disease states where IGF‐1 levels are low. Image content: The image shows GFAP positive primary astrocytes in culture (purple) with their nuclei stained with DAPI (blue), thereby validating our astrocyte cultures.Read the full article ‘Loss of insulin‐like growth factor‐1 signaling in astrocytes disrupts glutamate handling’ by D. Prabhu, S. M. Khan, K. Blackburn, J. P. Marshall, N. M. Ashpole ( J. Neurochem . 2019, vol. 151 (6), pp. 689–702) on doi: 10.1111/jnc.14879