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, November 2, 2015

Environmental enrichment enhances synaptic plasticity by internalization of striatal dopamine transporters

Well shit, this was written about in 2011 by Dr. Dale Corbett

enriched environment as talked about by Dr. Dale Corbett in 2011

How many times does the same information need to be repeated before our fucking failures of stroke associations take note and actually write up a stroke protocol on this. I bet the answer is that they never will do anything like this for survivors. Prove me wrong.

Environmental enrichment enhances synaptic plasticity by internalization of striatal dopamine transporters

  1. Myung-Sun Kim1,2,*
  2. Ji Hea Yu1,3,4,*
  3. Chul Hoon Kim4,5,6
  4. Jae Yong Choi5,7
  5. Jung Hwa Seo1,4
  6. Min-Young Lee1,2
  7. Chi Hoon Yi8
  8. Tae Hyun Choi8
  9. Young Hoon Ryu7
  10. Jong Eun Lee4,6,9
  11. Bae Hwan Lee4,6,10
  12. Hyongbum Kim5
  13. Sung-Rae Cho1,2,4,11⇑
  1. 1Department and Research Institute of Rehabilitation Medicine, Yonsei University College of Medicine, Seoul, Korea
  2. 2Yonsei Stem Cell Center, Avison Biomedical Research Center, Seoul, Korea
  3. 3Department of Medical Science, The Graduate School, Yonsei University, Seoul, Korea
  4. 4Brain Korea 21 PLUS Project for Medical Science, Yonsei University, Seoul, Korea
  5. 5Department of Pharmacology, Yonsei University College of Medicine, Seoul, Korea
  6. 6Brain Research Institute, Yonsei University College of Medicine, Seoul, Korea
  7. 7Department of Nuclear Medicine, Yonsei University College of Medicine, Seoul, Korea
  8. 8Department of Molecular Imaging, Korea Institute of Radiological and Medical Sciences, Seoul, Korea
  9. 9Department of Anatomy, Yonsei University College of Medicine, Seoul, Korea
  10. 10Department of Physiology, Yonsei University College of Medicine, Seoul, Korea
  11. 11Rehabilitation Institute of Neuromuscular Disease, Yonsei University College of Medicine, Seoul, Korea
  1. Sung-Rae Cho, Department and Research Institute of Rehabilitation Medicine, Yonsei University College of Medicine, 50 Yonsei-ro, Seodaemun-gu, Seoul 120-752, Korea. Email: srcho918@yuhs.ac
  1. ↵* These authors contributed equally to this work

Abstract

Environmental enrichment (EE) with a complex combination of physical, cognitive and social stimulations enhances synaptic plasticity and behavioral function. However, the mechanism remains to be elucidated in detail. We aimed to investigate dopamine-related synaptic plasticity underlying functional improvement after EE. For this, six-week-old CD-1 mice were randomly allocated to EE or standard conditions for two months. EE significantly enhanced behavioral functions such as rotarod and ladder walking tests. In a [18F]FPCIT positron emission tomography scan, binding values of striatal DAT were significantly decreased approximately 18% in the EE mice relative to the control mice. DAT inhibitor administrated to establish the relationship of the DAT down-regulation to the treatment effects also improved rotarod performances, suggesting that DAT inhibition recapitulated EE-mediated treatment benefits. Next, EE-induced internalization of DAT was confirmed using a surface biotinylation assay. In situ proximity ligation assay and immunoprecipitation demonstrated that EE significantly increased the phosphorylation of striatal DAT as well as the levels of DAT bound with protein kinase C (PKC). In conclusion, we suggest that EE enables phosphorylation of striatal DAT via a PKC-mediated pathway and causes DAT internalization. This is the first report to suggest an EE-mediated mechanism of synaptic plasticity by internalization of striatal DAT.

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