title: Nicotine modulates neurogenesis in the central canal during experimental autoimmune encephalomyelitis.
abstract: Nicotine has been shown to attenuate experimental autoimmune encephalomyelitis (EAE) through inhibiting inflammation in microglial populations during the disease course. In this study, we investigated whether nicotine modified the regenerative process in EAE by examining nestin-expressing neural stem cells (NSCs) in the spinal cord, which is the primary area of demyelination and inflammation in EAE. Our results show that the endogenous neurogenic responses in the spinal cord after EAE are limited and delayed: while nestin expression is increased, the proliferation of ependymal cells is inhibited compared to healthy animals. Nicotine application significantly reduced nestin expression and partially allowed for the proliferation of ependymal cells. We found that reduction of ependymal cell proliferation correlated with inflammation in the same area, which was relieved by the administration of nicotine. Further, increased numbers of oligodendrocytes (OLs) were observed after nicotine treatment. These findings give a new insight into the mechanism of how nicotine functions to attenuate EAE.
authors: Program in Neuroscience, Stony Brook University, Stony Brook, NY, United States; Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, United States.
authors: Z
authors: Z
authors: Gao
authors: Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, United States.
authors: J C
authors: JC
authors: Nissen
authors: Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, United States.
authors: L
authors: L
authors: Legakis
authors: Program in Neuroscience, Stony Brook University, Stony Brook, NY, United States; Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, United States. Electronic address: Styliani-anna.tsirka@stonybrook.edu.
authors: S E
authors: SE
authors: Tsirka
mesh_terms: D000818:Animals; D000941:Antigens / Q000378:metabolism; D000071183:Autophagy-Related Proteins; D000089622:Doublecortin Domain Proteins; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000139:chemically induced / Q000150:complications*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007249:Inflammation / Q000188:drug therapy / Q000209:etiology; D047908:Intracellular Signaling Peptides and Proteins / Q000378:metabolism; D019394:Ki-67 Antigen / Q000378:metabolism; D017493:Leukocyte Common Antigens / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D063308:Myelin-Oligodendrocyte Glycoprotein / Q000633:toxicity; D009410:Nerve Degeneration / Q000188:drug therapy* / Q000209:etiology* / Q000473:pathology; D064231:Nestin / Q000378:metabolism; D058953:Neural Stem Cells / Q000187:drug effects / Q000378:metabolism; D055495:Neurogenesis / Q000187:drug effects*; D009479:Neuropeptides / Q000378:metabolism; D009538:Nicotine / Q000627:therapeutic use*; D018722:Nicotinic Agonists / Q000627:therapeutic use*; D010446:Peptide Fragments / Q000633:toxicity; D011509:Proteoglycans / Q000378:metabolism; D013116:Spinal Cord / Q000473:pathology; D013997:Time Factors; D000099216:Chondroitin Sulfate Proteoglycan 4
chemical_list: D000941:Antigens; D000071183:Autophagy-Related Proteins; D000089622:Doublecortin Domain Proteins; D005904:Glial Fibrillary Acidic Protein; D047908:Intracellular Signaling Peptides and Proteins; D019394:Ki-67 Antigen; D017493:Leukocyte Common Antigens; D008869:Microtubule-Associated Proteins; D063308:Myelin-Oligodendrocyte Glycoprotein; D064231:Nestin; D009479:Neuropeptides; D009538:Nicotine; D018722:Nicotinic Agonists; D010446:Peptide Fragments; D011509:Proteoglycans; D000099216:Chondroitin Sulfate Proteoglycan 4; C428743:Rb1cc1 protein, mouse; C445081:myelin oligodendrocyte glycoprotein (35-55)
keywords: EAE; central canal; neural stem cells; nicotine; oligodendrocytes