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 role of the central nucleus of the amygdala in nociception--conditioned and unconditioned aversion--was studied. Rats received microinjection of vehicle or the N-type Ca2+ channel blocker omega-conotoxin GVIA (0.2 microg/250 nl) into the central amygdaloid nucleus prior to intra-plantar injection of formalin, ultrasound exposure or immediately prior to the acquisition phase of an aversive conditioning trial. Intra-amygdala omega-conotoxin GVIA resulted in an earlier onset of nociceptive response to formalin and increased nociceptive behaviour during the first 5 min. Omega-conotoxin GVIA significantly reduced conditioned freezing behaviour with no effect on ultrasound-induced unconditioned aversive behaviour. These data indicate that N-type Ca2+ channels in the central amygdaloid nucleus play a role in mediating behavioural responses to nociceptive and conditioned aversive stimuli.
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Source |
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http://dx.doi.org/10.1097/01.wnr.0000069062.85441.29 | DOI Listing |
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