Increased dendritic spine density sounds like something stroke survivors need to connect up damaged areas again. WHOM is going to do the human research on this and create useful rehab protocols? Don't start smoking on account of this. Ask your doctor if nicotine patches are adequate for delivering the nicotine needed.
Too bad the nicotine gum got cancelled.
Lei Fan, Huan Chen, Yong Liu, Hongwei Hou, Qingyuan Hu,
ERK signaling is required for nicotine-induced conditional place preference by regulating neuroplasticity genes expression in male mice,
Pharmacology Biochemistry and Behavior,
2022,
173510,
ISSN 0091-3057,
https://doi.org/10.1016/j.pbb.2022.173510.
(https://www.sciencedirect.com/science/article/pii/S0091305722001897)
Author links open overlay panel
- a
- Anhui
Institute of Optics and Fine Mechanics, Hefei Institutes of Physical
Science, Chinese Academy of Sciences, Hefei, Anhui, PR China
- b
- University of Science and Technology of China, Hefei, PR China
- c
- China National Tobacco Quality Supervision & Test Center, Zhengzhou, PR China
- d
- Key Laboratory of Tobacco Biological Effects, Zhengzhou, PR China
- e
- Joint Laboratory of Translational Neurobiology, Zhengzhou, PR China
Received 20 May 2022, Revised 12 December 2022, Accepted 13 December 2022, Available online 22 December 2022.
Highlights
- •
Pretreatment
with PD98059 blocks the establishment of nicotine CPP and the
expression of nicotine-induced synaptic plasticity-related genes in the
VTA and NAc.
- •
Activation of ERK1/2 and CREB is likely essential for expressing nicotine-induced synaptic plasticity-related proteins.
- •
Repeated exposure to nicotine promotes the complexity of dendritic morphology and increases the density of dendritic spine.
Abstract
Nicotine
is an addictive compound that interacts with nicotinic acetylcholine
receptors (nAChRs) in the ventral tegmental area (VTA), inducing a
release of dopamine in the nucleus accumbens (NAc). When neurons undergo
repeated exposure to nicotine, several adaptive changes in
neuroplasticity occur. Activation of nAChRs involves numerous
intracellular signaling cascades that likely contribute to
neuroplasticity and ultimately the establishment of nicotine addiction.
Nevertheless, the molecular mechanisms underlying this adaptation remain
unclear. To explore the effects of nicotine on neuroplasticity, a
stable nicotine-induced conditioned place preference (CPP) model was
constructed by intravenous injection in mice. Using a PCR array, we
observed significant changes in the expression of synaptic
plasticity-related genes in the VTA (16 mRNAs) and NAc (40 mRNAs). When
mice were pre-treated with PD98059, an extracellular signal-regulated
kinase (ERK) inhibitor, more gene expression changes in the VTA (53
mRNAs) and NAc (60 mRNAs) were found. Moreover, PD98059 pre-treatment
blocked the increased p-ERK/ERK and p-CREB/CREB ratios and decreased the
expression of synaptic plasticity-related proteins such as SAP102,
PSD95, synaptophysin, and BDNF, these changes might contribute to
preventing the establishment of nicotine-induced CPP. Furthermore,
neurons from the VTA and NAc of nicotine CPP mice had an increased
dendritic spine density and complexity of dendritic morphology by Golgi
staining. PD98059 also blocked this dynamic. These results demonstrate
that repeated exposure to nicotine may remold the expression of
neuroplasticity-related genes by activating the ERK signaling pathway in
the VTA and NAc, and is related to the establishment of
nicotine-induced CPP.
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