Intracisternal administration of COX inhibitors attenuates mechanical allodynia following compression of the trigeminal ganglion in rats
The purpose of the present study was to investigate the role of central cyclooxygenase (COX) pathways in the modulation of mechanical allodynia following compression of the left trigeminal ganglion. Experiments were carried out on male Sprague–Dawley rats mounted onto a stereotaxic frame under anest...
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Published in | Progress in neuro-psychopharmacology & biological psychiatry Vol. 33; no. 4; pp. 589 - 595 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Amsterdam
Elsevier Inc
15.06.2009
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | The purpose of the present study was to investigate the role of central cyclooxygenase (COX) pathways in the modulation of mechanical allodynia following compression of the left trigeminal ganglion. Experiments were carried out on male Sprague–Dawley rats mounted onto a stereotaxic frame under anesthesia. For compression, a 4% agar solution (10 μl) was injected into the trigeminal ganglion. In the control group, rats were sham operated without agar injections. Ipsilateral and contralateral air-puff thresholds significantly decreased following trigeminal ganglion compression. Mechanical allodynia was established within 3 days and lasted beyond postoperative day 30, returning to preoperative levels at approximately 55 days following compression. Intracisternal administration of indomethacin, a non-selective COX inhibitor, SC-560, a selective COX-1 inhibitor, or NS-398, a selective COX-2 inhibitor, significantly inhibited mechanical allodynia. The individual anti-allodynic effects of the three COX inhibitors persisted for 6 h and returned to pretreatment values within 24 h. Based on these results, the blockade of central COX pathways may comprise a potential new therapeutic tool for the treatment of trigeminal ganglion compression-induced nociception. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0278-5846 1878-4216 |
DOI: | 10.1016/j.pnpbp.2009.02.010 |