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: 1034
Function: getPubMedXML
File: /var/www/html/application/helpers/my_audit_helper.php
Line: 3152
Function: GetPubMedArticleOutput_2016
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
Modification of the number of GABA(A) receptors (GABA(A)Rs) clustered at inhibitory synapses can regulate inhibitory synapse strength with important implications for information processing and nervous system plasticity and pathology. Currently, however, the mechanisms that regulate the number of GABA(A)Rs at synapses remain poorly understood. By imaging superecliptic pHluorin tagged GABA(A)R subunits we show that synaptic GABA(A)R clusters are normally stable, but that increased neuronal activity upon glutamate receptor (GluR) activation results in their rapid and reversible dispersal. This dispersal correlates with increases in the mobility of single GABA(A)Rs within the clusters as determined using single-particle tracking of GABA(A)Rs labeled with quantum dots. GluR-dependent dispersal of GABA(A)R clusters requires Ca(2+) influx via NMDA receptors (NMDARs) and activation of the phosphatase calcineurin. Moreover, the dispersal of GABA(A)R clusters and increased mobility of individual GABA(A)Rs are dependent on serine 327 within the intracellular loop of the GABA(A)R γ2 subunit. Thus, NMDAR signaling, via calcineurin and a key GABA(A)R phosphorylation site, controls the stability of synaptic GABA(A)Rs, with important implications for activity-dependent control of synaptic inhibition and neuronal plasticity.
Download full-text PDF |
Source |
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2944765 | PMC |
http://dx.doi.org/10.1073/pnas.1000589107 | DOI Listing |
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