Nicotine Neurotoxicity Involves Low Wnt1 Signaling in Spinal Locomotor Networks of the Postnatal Rodent Spinal Cord

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Nicotine Neurotoxicity Involves Low Wnt1 Signaling in Spinal Locomotor Networks of the Postnatal Rodent Spinal Cord. / Kaur, Jaspreet; Mazzone, Graciela L ; Aquino, Jorge B ; Nistri, Andrea.

In: International Journal of Molecular Sciences (CD-ROM), Vol. 22, No. 17, 03.09.2021, p. 1-21.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Kaur, J, Mazzone, GL, Aquino, JB & Nistri, A 2021, 'Nicotine Neurotoxicity Involves Low Wnt1 Signaling in Spinal Locomotor Networks of the Postnatal Rodent Spinal Cord', International Journal of Molecular Sciences (CD-ROM), vol. 22, no. 17, pp. 1-21. https://doi.org/10.3390/ijms22179572

APA

Kaur, J., Mazzone, G. L., Aquino, J. B., & Nistri, A. (2021). Nicotine Neurotoxicity Involves Low Wnt1 Signaling in Spinal Locomotor Networks of the Postnatal Rodent Spinal Cord. International Journal of Molecular Sciences (CD-ROM), 22(17), 1-21. https://doi.org/10.3390/ijms22179572

Vancouver

Kaur J, Mazzone GL, Aquino JB, Nistri A. Nicotine Neurotoxicity Involves Low Wnt1 Signaling in Spinal Locomotor Networks of the Postnatal Rodent Spinal Cord. International Journal of Molecular Sciences (CD-ROM). 2021 Sep 3;22(17):1-21. https://doi.org/10.3390/ijms22179572

Author

Kaur, Jaspreet ; Mazzone, Graciela L ; Aquino, Jorge B ; Nistri, Andrea. / Nicotine Neurotoxicity Involves Low Wnt1 Signaling in Spinal Locomotor Networks of the Postnatal Rodent Spinal Cord. In: International Journal of Molecular Sciences (CD-ROM). 2021 ; Vol. 22, No. 17. pp. 1-21.

Bibtex

@article{6cf0871509934a3e81b4c27cbd3af9c5,
title = "Nicotine Neurotoxicity Involves Low Wnt1 Signaling in Spinal Locomotor Networks of the Postnatal Rodent Spinal Cord",
abstract = "The postnatal rodent spinal cord in-vitro is a useful model to investigate early pathophysiological changes after injury. While low dose nicotine (1 µM) induces neuroprotection, how higher doses affect spinal networks is unknown. Using spinal preparations of postnatal wild-type Wistar rat and Wnt1Cre2:Rosa26Tom double-transgenic mouse, we studied the effect of nicotine (0.5–10 µM) on locomotor networks in-vitro. Nicotine 10 µM induced motoneuron depolarization, suppressed monosynaptic reflexes, and decreased fictive locomotion in rat spinal cord. Delayed fall in neuronal numbers (including motoneurons) of central and ventral regions emerged without loss of dorsal neurons. Conversely, nicotine (0.5–1 µM) preserved neurons throughout the spinal cord and strongly activated the Wnt1 signaling pathway. High-dose nicotine enhanced expression of S100 and GFAP in astrocytes indicating a stress response. Excitotoxicity induced by kainate was contrasted by nicotine (10 µM) in the dorsal area and persisted in central and ventral regions with no change in basal Wnt signaling. When combining nicotine with kainate, the activation of Wnt1 was reduced compared to kainate/sham. The present results suggest that high dose nicotine was neurotoxic to central and ventral spinal neurons as the neuroprotective role of Wnt signaling became attenuated. This also corroborates the risk of cigarette smoking for the foetus/newborn since tobacco contains nicotine. ",
keywords = "Faculty of Health and Medical Sciences",
author = "Jaspreet Kaur and Mazzone, {Graciela L} and Aquino, {Jorge B} and Andrea Nistri",
year = "2021",
month = sep,
day = "3",
doi = "10.3390/ijms22179572",
language = "English",
volume = "22",
pages = "1--21",
journal = "International Journal of Molecular Sciences (CD-ROM)",
issn = "1424-6783",
publisher = "M D P I AG",
number = "17",

}

RIS

TY - JOUR

T1 - Nicotine Neurotoxicity Involves Low Wnt1 Signaling in Spinal Locomotor Networks of the Postnatal Rodent Spinal Cord

AU - Kaur, Jaspreet

AU - Mazzone, Graciela L

AU - Aquino, Jorge B

AU - Nistri, Andrea

PY - 2021/9/3

Y1 - 2021/9/3

N2 - The postnatal rodent spinal cord in-vitro is a useful model to investigate early pathophysiological changes after injury. While low dose nicotine (1 µM) induces neuroprotection, how higher doses affect spinal networks is unknown. Using spinal preparations of postnatal wild-type Wistar rat and Wnt1Cre2:Rosa26Tom double-transgenic mouse, we studied the effect of nicotine (0.5–10 µM) on locomotor networks in-vitro. Nicotine 10 µM induced motoneuron depolarization, suppressed monosynaptic reflexes, and decreased fictive locomotion in rat spinal cord. Delayed fall in neuronal numbers (including motoneurons) of central and ventral regions emerged without loss of dorsal neurons. Conversely, nicotine (0.5–1 µM) preserved neurons throughout the spinal cord and strongly activated the Wnt1 signaling pathway. High-dose nicotine enhanced expression of S100 and GFAP in astrocytes indicating a stress response. Excitotoxicity induced by kainate was contrasted by nicotine (10 µM) in the dorsal area and persisted in central and ventral regions with no change in basal Wnt signaling. When combining nicotine with kainate, the activation of Wnt1 was reduced compared to kainate/sham. The present results suggest that high dose nicotine was neurotoxic to central and ventral spinal neurons as the neuroprotective role of Wnt signaling became attenuated. This also corroborates the risk of cigarette smoking for the foetus/newborn since tobacco contains nicotine.

AB - The postnatal rodent spinal cord in-vitro is a useful model to investigate early pathophysiological changes after injury. While low dose nicotine (1 µM) induces neuroprotection, how higher doses affect spinal networks is unknown. Using spinal preparations of postnatal wild-type Wistar rat and Wnt1Cre2:Rosa26Tom double-transgenic mouse, we studied the effect of nicotine (0.5–10 µM) on locomotor networks in-vitro. Nicotine 10 µM induced motoneuron depolarization, suppressed monosynaptic reflexes, and decreased fictive locomotion in rat spinal cord. Delayed fall in neuronal numbers (including motoneurons) of central and ventral regions emerged without loss of dorsal neurons. Conversely, nicotine (0.5–1 µM) preserved neurons throughout the spinal cord and strongly activated the Wnt1 signaling pathway. High-dose nicotine enhanced expression of S100 and GFAP in astrocytes indicating a stress response. Excitotoxicity induced by kainate was contrasted by nicotine (10 µM) in the dorsal area and persisted in central and ventral regions with no change in basal Wnt signaling. When combining nicotine with kainate, the activation of Wnt1 was reduced compared to kainate/sham. The present results suggest that high dose nicotine was neurotoxic to central and ventral spinal neurons as the neuroprotective role of Wnt signaling became attenuated. This also corroborates the risk of cigarette smoking for the foetus/newborn since tobacco contains nicotine.

KW - Faculty of Health and Medical Sciences

UR - https://www.mdpi.com/1422-0067/22/17/9572

U2 - 10.3390/ijms22179572

DO - 10.3390/ijms22179572

M3 - Journal article

C2 - 34502498

VL - 22

SP - 1

EP - 21

JO - International Journal of Molecular Sciences (CD-ROM)

JF - International Journal of Molecular Sciences (CD-ROM)

SN - 1424-6783

IS - 17

ER -

ID: 275790571