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However, the identity of Ca\n                    <jats:sup>2<\/jats:sup>\n                    + channels and the mechanisms underlying neurotoxin\u2010induced neuronal degeneration are not well understood. In this study, the dopaminergic neurotoxins 6\u2010hydroxydopamine (6\u2010OHDA) and 1\u2010methyl\u20104\u2010phenylpyridium ions (MPP+)\/1\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine (MPTP), which mimic Parkinson's disease (PD), induced neuronal degeneration by decreasing store\u2010mediated Ca\n                    <jats:sup>2<\/jats:sup>\n                    + entry. The function of the transient receptor potential canonical (TRPC)\u20101 channel was decreased upon exposure to the neurotoxins, followed by a decrease in TRPC1 expression. Similar to neurotoxins, samples from patients with PD exhibited attenuated TRPC1 expression, which was accompanied by a decrease in autophagic markers and a subsequent increase in apoptosis markers. Furthermore, exposure to neurotoxins attenuated PKC phosphorylation, decreased expression of autophagic markers, and increased apoptosis in SHSY\u20105Y neu\u2010roblastoma cells, which was again dependent on TRPC1. Prolonged neurotoxin treatment attenuated the binding of NF\u2010\u03baB to the TRPC1 promoter, which resulted in a decrease in TRPC1 expression, thereby attenuating autophagy and activating cell death. Restoration of TRPC1 expression rescued the effects of the dopaminergic neurotoxins in neu\u2010roblastoma cells by increasing Ca\n                    <jats:sup>2<\/jats:sup>\n                    + entry, restoring NF\u2010\u039aB activity, and promoting autophagy. Overall, these results suggest that dopaminergic neurotoxins initially decreased Ca\n                    <jats:sup>2<\/jats:sup>\n                    + entry, which inhibited the binding of NF\u2010\u03baB to the TRPC1 promoter, thereby inhibiting TRPC1 expression and resulting in cell death by preventing autophagy.\u2014 Sukumaran, P., Sun, Y., Antonson, N., Singh, B. B. Dopaminergic neurotoxins induce cell death by attenuating NF\u2010\u03baB\u2010mediated regulation of TRPC1 expression and autophagy. FASEB J. 32,1640\u20101652 (2018).\n                    <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/www.fasebj.org\">www.fasebj.org<\/jats:ext-link>\n                  <\/jats:p>","DOI":"10.1096\/fj.201700662rr","type":"journal-article","created":{"date-parts":[[2017,11,17]],"date-time":"2017-11-17T11:15:32Z","timestamp":1510917332000},"page":"1640-1652","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":36,"title":["Dopaminergic neurotoxins induce cell death by attenuating NF\u2010\u03baB\u2010mediated regulation of TRPC1 expression and autophagy"],"prefix":"10.1096","volume":"32","author":[{"given":"Pramod","family":"Sukumaran","sequence":"first","affiliation":[{"name":"Department of Biomedical Science School of Medicine and Health Sciences University of North Dakota Grand Forks North Dakota 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