Severity: Warning
Message: file_get_contents(https://...@pubfacts.com&api_key=b8daa3ad693db53b1410957c26c9a51b4908&a=1): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
Filename: helpers/my_audit_helper.php
Line Number: 176
Backtrace:
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 176
Function: file_get_contents
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 250
Function: simplexml_load_file_from_url
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3122
Function: getPubMedXML
File: /var/www/html/application/controllers/Detail.php
Line: 575
Function: pubMedSearch_Global
File: /var/www/html/application/controllers/Detail.php
Line: 489
Function: pubMedGetRelatedKeyword
File: /var/www/html/index.php
Line: 316
Function: require_once
The mature central nervous system has a very limited capacity to repair itself after injury or disease, often leading to lifelong disabilities. Two key questions in neurobiology are why the brain has such limited plasticity, and how we could enhance it. There has been extensive research on how external inhibitors, present in the mature central nervous system, cooperate to restrict neurite plasticity-the ability of neurons to sprout and reorganize their connections. In a recent article, we have described an unsuspected mechanism by which neurons control (and actually repress) their capacity to sprout in a cell-autonomous manner. Our discovery implies that protrusive potential is not lost in mature neurons but internally repressed. This discovery opens up new research avenues and has a strong potential from a translational standpoint. Here I review our previous results and propose a more general hypothesis on the molecular mechanisms controlling neurite plasticity.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2734034 | PMC |
http://dx.doi.org/10.4161/cib.2.4.8309 | DOI Listing |
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