Deans' stroke musings: Sodium channel gating modifier promotes neuronal repair and functional recovery from ischemic stroke. E Sequeira

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.

Wednesday, May 13, 2020

Sodium channel gating modifier promotes neuronal repair and functional recovery from ischemic stroke. E Sequeira - 2020

Pretty impressive coming from a Ph.D student. Now we just need our non-existent stroke leaders to get followup human research done. That will never occur, we have NO STROKE LEADERS.

Sodium channel gating modifier promotes neuronal repair and functional recovery from ischemic stroke.

Abstract

Ischemic stroke is a leading cause of adult disability, which presents a pressing
need for a pharmacological therapy. Emerging literature suggests that after a stroke, the
peri-infarct region exhibits dynamic changes in excitability. The acute ischemic phase
triggers glutamate-mediated excitotoxic neuronal death. On the contrary, during the
chronic phase, when the brain begins to repair itself, it displays heightened
neuroplasticity that also resembles the neuronal developmental stages. However, this
recovery is incomplete. Thus, promoting cortical excitability during the repair and
recovery phase could potentially be therapeutic. Brevetoxin-2 (PbTx-2), a voltage-gated
sodium channel (VGSC) modifier, increases intracellular sodium ([Na+]i), upregulates N
methyl-d-aspartate receptors (NMDAR) channel activity, and engages activity-dependent
downstream calcium (Ca2+) signaling pathways. In immature cerebrocortical neurons,
PbTx-2 promoted neuronal structural plasticity by increasing neurite outgrowth,
dendritogenesis and synaptogenesis. This led us to hypothesize that PbTx-2 could
promote structural remodeling of neural networks in the peri-infarct site and subsequently
promote functional outcomes after stroke. In the current study, we have investigated this
phenomenon using adult male transgenic yellow fluorescent protein expressing (YFP)
mice by providing an epicortical application of PbTx-2 five days after inducing a
photothrombotic stroke. We show that PbTx-2 enhanced dendritic arbor complexity and
excitatory synapse density of the cortical layer V pyramidal neurons in the peri-infarct
cortex. Consistent with increased neuronal plasticity, PbTx-2 also produced a robust gain
of motor recovery. Collectively, our results identify an activity-dependent pharmacologic
strategy to promote recovery from stroke and possibly other brain injuries.