PMID: 9539675Apr 16, 1998Paper

Attenuation of IGF-1 antinociceptive action and a reduction in spinal cord gene expression of its receptor in experimental diabetes

Pain
M S Bitar, C W Pilcher

Abstract

Insulin-like growth factor I (IGF-1) is trophic to sensory, motor and sympathetic neurons. Intrathecal (i.t.) administration of IGF-1 produced analgesic effects when tail flick/withdrawal latency was used as an indicator. This action was blocked by genistein (an inhibitor of tyrosine kinase) but not by atipamezol (an alpha2 adrenoreceptor antagonist), naloxone (an opioid antagonist) or glibenclamide (a blocker of ATP sensitive K+ channels). Induction of diabetes with streptozotocin (STZ, 55 mg/kg, i.v.) impaired the ability of IGF-1 to elevate nociceptive threshold. This phenomenon was not seen in normal animals rendered hyperglycemic with D-glucose (20 mmol in 2.5 ml of saline, i.p.). PCR-based assay revealed that the lumbar region of the spinal cord expresses mRNA transcripts for IGF-1 and its receptor. The rates of expression of both of these transcripts were reduced during diabetes. The above behavioral and biochemical abnormalities induced by the diabetic state were partially restored following replacement therapy with insulin. Overall, our data suggest that a receptor-linked tyrosine kinase mediates the antinociceptive effect of IGF-1. Additionally, the attenuation in the ability of IGF-1 to elevate nociceptive threshold ...Continue Reading

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Citations

Nov 26, 2002·Annals of Neurology·Matthew J CranerStephen G Waxman
Dec 12, 2002·Trends in Endocrinology and Metabolism : TEM·Gordon Blackburn-Munro, Ruth Blackburn-Munro
Aug 23, 2008·Endocrinology·Kelli A SullivanEva L Feldman
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Nov 19, 2003·The Journal of Pain : Official Journal of the American Pain Society·J S Mogil, K E McCarson

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