Deans' stroke musings: Melatonin ameliorates neural function by promoting endogenous neurogenesis through MT2 melatonin receptor in ischemic stroke 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.

Tuesday, February 21, 2012

Melatonin ameliorates neural function by promoting endogenous neurogenesis through MT2 melatonin receptor in ischemic stroke mice.

Another hyperacute possibility, but it doesn't say how it was administered.
http://www.ncbi.nlm.nih.gov/pubmed/22330064

Abstract

Melatonin has many protective effects against ischemic stroke, but the underlying neuroprotective mechanisms are not fully understood. Our aim was to explore the relationship between melatonin's neuroprotective effects and activation of the MT2 melatonin receptor in a murine ischemic stroke model. Male ICR mice were subjected to a transient middle cerebral ischemic/reperfusional injury and melatonin (5 and 10mg/kg, i.p.) was administrated once daily starting 2h after ischemia. More than 80% of the mice died within 5days after stroke without treatment. Melatonin treatment significantly improved the survival rates and neural functioning with modestly prolonged lifespan of the stroke mice by preserving blood-brain barrier (BBB) integrity via a reduction in the enormous amount of stroke-induced free radical production and significant gp91(phox) cell infiltration. These protective effects of melatonin were reversed by pretreatment with MT2 melatonin receptor antagonists (4-phenyl-2-propionamidotetralin (4P-PDOT) and luzindole). Moreover, treatment with melatonin after stroke dramatically enhanced endogenous neurogenesis (doublecortin-positive) and cell proliferation (ki67-positive) in the peri-infarct regions. Most ki67-positive cells were nestin-positive and NG2-positive neural stem/progenitor cells that co-expressed two neurodevelopmental proteins (adam11 and adamts20) and MT2 melatonin receptor. RT-PCR revealed that the gene expression level of doublecortin, ki67, adamts20 and adam11 are markedly reduced by stroke, but are restored by melatonin treatment; furthermore, pretreatment with 4P-PDOT and luzindole antagonized melatonin's restorative effect. Our results support the hypothesis that melatonin is able to protect mice against stroke by activating MT2 melatonin receptors, which reduces oxidative/inflammatory stress. This results in the preservation of BBB integrity and enhances endogenous neurogenesis by up-regulating neurodevelopmental gene/protein expression.