We have previously reported that metabolites of catecholamines contribute to the enhanced mechanical sensitivity of primary sensory afferents in a model of alcoholic neuropathy (Dina et al., 2008);. Because epinephrine and norepinephrine are preferentially metabolized by MAO-A, and a MAO-A inhibitor reduced pain in our model of alcoholic neuropathy, we tested the effect on nociception of a metabolite implicated in neurodegenerative diseases of the central nervous system, 3,4 dihydroxyphenylglycolaldehyde (Dopegal). To confirm its identity we performed a molecular characterization. According to the results obtained by proton nuclear magnetic resonance spectroscopy, gas chromatography coupled mass spectrometry, high performance liquid chromatography and matrix-assisted laser desorption ionization time-of flight mass spectrometry we determined that the sample consisted of at least three different compounds including Dopegal and the methylester of its corresponding acid 3,4 dihydroxymandelic acid (data not shown). Because we cannot rule out the possibility that the sample/batch of Dopegal that we were using to demonstrate the hyperalgesic effect of catecholamine metabolites was contaminated as well, we are requesting that the evidence be withdrawn as described in Figure 4 along with the description of the hyperalgesic effects of Dopegal for our publication ‘Neurotoxic catecholamine metabolite in nociceptors contribute to painful peripheral neuropathy’ (Dina et al., 2008). We would like to acknowledge the help of Drs David Goldstein and Noel Whittaker of the NIH, Dr Oliver Bogen at UCSF and Professor Stefan Hecht, Department of Organic Chemistry, Humbolt University, Berlin in performing the chemical characterizations.


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