AI Article Synopsis

  • The study aimed to investigate how insulin-like growth factor-1 (IGF-1) affects the expression of specific mRNAs related to substance P and calcitonin gene-related peptide in nerve cells under stress from glutamate.
  • The researchers cultured dorsal root ganglion (DRG) neurons from rats and exposed them to glutamate with varying concentrations of IGF-1 to assess the impact on neuron health and gene expression.
  • Results indicated that IGF-1 not only prevented neuron damage caused by glutamate but also increased the mRNA levels of substance P and calcitonin gene-related peptide in a dose-dependent manner, suggesting a potential neuroprotective role for IGF-1.

Article Abstract

Objective: To determine the effects of insulin-like growth factor-1 (IGF-1) on the expression of preprotachykinin (PPT) mRNA encoding substance P (SP) and calcitonin gene-related peptide (CGRP) mRNA in cultured dorsal root ganglion (DRG) neurons with excitotoxicity induced by glutamate (Glu).

Methods: DRGs were dissected from embryonic day 15 Wistar rats. DRG neurons were dissociated and cultured for 48 h and then exposed to Glu (0.2 mmol/L) or Glu (0.2 mmol/L) plus IGF-1 (5 nmol/L, 10 nmol/L and 20 nmol/L) for 12 h. The DRG neurons in control group were exposed to only growth media throughout the experiment. After that, the living DRG neurons were observed under inverted phase contrast microscope and microphotographs were taken. The expression levels of PPT and CGRP mRNAs were detected by reverse transcription-polymerase chain reaction (RT-PCR).

Results: IGF-1 could inhibit Glu-induced shortening of neurite. Besides, IGF-1 could significantly increase the levels of PPT mRNA and CGRP mRNA in primary cultured DRG neurons with Glu-induced excitotoxicity, in a dose-dependent manner.

Conclusion: IGF-1 may exert neuroprotective effects on DRG neurons against Glu-induced excitotoxicity, probably through regulating the expression levels of PPT and CGRP mRNAs.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5560371PMC
http://dx.doi.org/10.1007/s12264-010-9142-0DOI Listing

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