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The rat rotenone model reproduces many of the pathological features of the human disease, including apomorphine\u2010responsive behavioral deficits, DA depletion, loss of striatal DA terminals and nigral dopaminergic neurons, and \u03b1\u2010synuclein\/polyubiquitin\u2010positive cytoplasmic inclusions reminiscent of Lewy bodies. Therefore, this model is well\u2010suited to examine potential neuroprotective agents. Melatonin is produced mainly by the pineal gland and is known primarily for regulating circadian rhythms. It also has potent free radical scavenging and antiinflammatory properties. Melatonin has been reported to be neuroprotective in the 6\u2010hydroxydopamine (6\u2010OHDA) and 1\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine (MPTP) models of PD. However, there are conflicting reports suggesting that melatonin does not provide neuroprotection in these models. Melatonin elicits significant functional changes in the nigrostriatal DA system that may affect 6\u2010OHDA and MPTP entry into cells. Therefore, rotenone is an ideal model for assessing protection, because it does not rely on the dopamine transporter uptake to exert neurotoxicity. In this study, the neuroprotective potential of melatonin in the rotenone PD model was assessed. Melatonin potentiated striatal catecholamine depletion, striatal terminal loss, and nigral DA cell loss. Indeed, melatonin alone elicited alterations in striatal catecholamine content. Our findings indicate that melatonin is not neuroprotective in the rotenone model of PD and may exacerbate neurodegeneration. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.22201","type":"journal-article","created":{"date-parts":[[2009,8,13]],"date-time":"2009-08-13T17:25:27Z","timestamp":1250184327000},"page":"420-427","source":"Crossref","is-referenced-by-count":78,"title":["Melatonin treatment potentiates neurodegeneration in a rat rotenone Parkinson's disease model"],"prefix":"10.1002","volume":"88","author":[{"given":"Victor","family":"Tapias","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jason R.","family":"Cannon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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