Abstract
AbstractIn rats, diabetes causes an increase in the frequency of biphasic flinching behavior following paw formalin injection. We now report that diabetic rats exhibit a protracted monophasic period of flinching behavior in response to lower (0.2%) concentrations of formalin, that do not stimulate control rats. Allodynia developed within one week of diabetes was not prevented by aldose reductase inhibition or alleviated by intrathecal MK801, but was dose-dependently reduced by intrathecal delivery of indomethacin. This novel model of diabetic allodynia may serve as a screening tool for potential therapeutic agents targeted at painful diabetic neuropathy and allow investigation of mechanisms by which diabetes induces allodynia.
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