Deans' stroke musings: ERK signaling is required for nicotine-induced conditional place preference by regulating neuroplasticity genes expression in male mice

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Saturday, December 24, 2022

ERK signaling is required for nicotine-induced conditional place preference by regulating neuroplasticity genes expression in male mice

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)

^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.

https://doi.org/10.1016/j.pbb.2022.173510 Get rights and content

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.