Deans' stroke musings: Melatonin improves neuroplasticity by upregulating the growth-associated protein 43 (GAP-43) and NMDAR-post-synaptic density-95 (PSD95) proteins in cultured neurons exposed to glutamate excitotoxicity and in rats subjected to transient focal cerebral ischemia even during a long-term recovery period

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, December 23, 2013

Melatonin improves neuroplasticity by upregulating the growth-associated protein 43 (GAP-43) and NMDAR-post-synaptic density-95 (PSD95) proteins in cultured neurons exposed to glutamate excitotoxicity and in rats subjected to transient focal cerebral ischemia even during a long-term recovery period

This is listed in my 31 things I'm going to demand my doctor give me in the first week. More proof to get this done. I'm sure your doctor subscribes to the Journal of Pineal Research.
http://onlinelibrary.wiley.com/doi/10.1111/jpi.12114/abstract

Wei-Sheng Juan^1,†,
Sheng-Yang Huang^1,†,
Che-Chao Chang¹,
Yu-Chang Hung¹,
Yu-Wen Lin¹,
Tsung-Ying Chen^1,2,
Ai-Hua Lee¹,
Ai-Chiang Lee¹,
Tian-Shung Wu^1,3,
E-Jian Lee^1,*

DOI: 10.1111/jpi.12114

Issue

Journal of Pineal Research

Accepted Article (Accepted, unedited articles published online and citable. The final edited and typeset version of record will appear in future.)

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Author Information Publication History

This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1111/jpi.12114

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Abstract
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Keywords:

Stroke;
glutamate excitotoxicity;
neuroplasticity;
neuroprotection;
melatonin

Abstract

Recent evidence shows that the NMDAR-post-synaptic density-95 (PSD95), growth-associated protein 43 (GAP-43) and matrix metalloproteinase-9 (MMP-9) protein enhance neuroplasticity at the subacute stage of stroke. Here, we evaluated whether melatonin would modulate the PSD95, GAP-43 and MMP-9 proteins in cultured neurons exposed to glutamate excitotoxicity and in rats subjected to experimental stroke. Adult male Sprague-Dawley rats were treated with melatonin (5 mg/kg) or vehicle at reperfusion onset after transient occlusion of the right middle cerebral artery (tMCAO) for 90 min. Animals were euthanized for Western immunoblot analyses for the PSD-95 and GAP-43 proteins and gelatin zymography for the MMP-9 activity at 7-day post-insult. Another set of animals was sacrificed for histologic and Golgi-Cox-impregnated sections at 28 days post-insult. In cultured neurons exposed to glutamate excitotoxicity, melatonin significantly up-regulated the GAP-43 and PSD-95 expressions and improved dendritic aborizations (P < 0.05, respectively). Relative to controls, melatonin-treated stroke animals caused a significant improvement of GAP-43 and PSD-95 expressions as well as the MMP-9 activity in the ischemic brain (P < 0.05). Consequently, melatonin also significantly promoted the dendritic spine density and reduced infarction in the ischemic brain, and improved neurobehaviors as well at 28 days post-insult (P < 0.05, respectively). Together, melatonin upregulates GAP-43, PSD-95 and MMP-9 proteins, which likely accounts for its actions to improve neuroplasticity in cultured neurons exposed to glutamate excitotoxicity, and to enhance long-term neuroprotection, neuroplasticity and brain remodeling in stroke rats.