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.

Monday, April 19, 2021

Functional Activation of Newborn Neurons Following Alcohol-Induced Reactive Neurogenesis

I would not suggest you use this method to get neurogenesis going.

Functional Activation of Newborn Neurons FollowingAlcohol-Induced Reactive Neurogenesis

Natalie N. Nawarawong 1,†, Chelsea G. Nickell 2,†, Deann M. Hopkins 2
, James R. Pauly 2
and Kimberly Nixon 1,2,*


Citation: Nawarawong, N.N.;
Nickell, C.G.; Hopkins, D.M.; Pauly,
J.R.; Nixon, K. Functional Activation
of Newborn Neurons Following
Alcohol-Induced Reactive
Neurogenesis. Brain Sci. 2021, 11, 499.
https://doi.org/10.3390/brainsci
11040499
Academic Editor: Chitra Mandyam
Received: 17 March 2021
Accepted: 11 April 2021
Published: 15 April 2021
Publisher’s Note: MDPI stays neutral
with regard to jurisdictional claims in
published maps and institutional affiliations.
Copyright: © 2021 by the authors.
Licensee MDPI, Basel, Switzerland.
This article is an open access article
distributed under the terms and
conditions of the Creative Commons
Attribution (CC BY) license (https://
creativecommons.org/licenses/by/
4.0/).
1 College of Pharmacy, The University of Texas at Austin, Austin, TX 78712, USA;
natalie.nawarawong@austin.utexas.edu
2 Department of Pharmaceutical Sciences, University of Kentucky, Lexington, KY 40536, USA;
Chelsea.nickell@uky.edu (C.G.N.); dmhopk1@uky.edu (D.M.H.); jim.pauly@uky.edu (J.R.P.)
* Correspondence: Kim.nixon@austin.utexas.edu; Tel.: +1-512-232-2788
† These authors contributed equally to this work.

Abstract: 

Abstinence after alcohol dependence leads to structural and functional recovery in many
regions of the brain, especially the hippocampus. Significant increases in neural stem cell (NSC) proliferation and subsequent “reactive neurogenesis” coincides with structural recovery in hippocampal
dentate gyrus (DG). However, whether these reactively born neurons are integrated appropriately
into neural circuits remains unknown. Therefore, adult male rats were exposed to a binge model of
alcohol dependence. On day 7 of abstinence, the peak of reactive NSC proliferation, rats were injected
with bromodeoxyuridine (BrdU) to label dividing cells. After six weeks, rats underwent Morris
Water Maze (MWM) training then were sacrificed ninety minutes after the final training session.
Using fluorescent immunohistochemistry for c-Fos (neuronal activation), BrdU, and Neuronal Nuclei
(NeuN), we investigated whether neurons born during reactive neurogenesis were incorporated into
a newly learned MWM neuronal ensemble. Prior alcohol exposure increased the number of BrdU+
cells and newborn neurons (BrdU+/NeuN+ cells) in the DG versus controls. However, prior ethanol
exposure had no significant impact on MWM-induced c-Fos expression. Despite increased BrdU+
neurons, no difference in the number of activated newborn neurons (BrdU+/c-Fos+/NeuN+) was
observed. These data suggest that neurons born during alcohol-induced reactive neurogenesis are
functionally integrated into hippocampal circuitry

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