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| Title: | The Antiallodynic Action Target of Intrathecal Gabapentin: Ca2+ Channels, K-Atp Channels or N-Methyl-D-Aspartic Acid Receptors? |
| Authors: | 鄭仁坤;邱麗珠
CHENG, JEN-KUN;CHIOU, LIH-CHU |
| Contributors: | 藥理學科所 |
| Keywords: | SENSITIVE POTASSIUM CHANNELS;RAT MODEL;TACTILE ALLODYNIA;CALCIUM-CHANNELS;NEUROPATHIC PAIN;NEURONS |
| Date: | 2006 |
| Issue Date: | 2009-09-23T08:44:05Z |
| Abstract: | Gabapentin is a novel analgesic whose mechanism of action is not known. We investigated in a postoperative pain model whether adenosine triphosphate (ATP)sensitive K+ (K-ATP) channels, N-methyl-D-aspartic acid (NMDA) receptors, and Ca2 + channels are involved in the antiallodynic effect of intrathecal gabapentin. Mechanical allodynia was induced by a paw incision in isoflurane-anesthetized rats. Withdrawal thresholds to von Frey filament stimulation near the incision site were measured before and after incision and after intrathecal drug administration. The antiallodynic effect of gabapentin (100 mu g) was not affected by intrathecal pretreatment with antagonists of K-ATP channels, NMDA receptors or gamma-aminobutyric acid (GABA), receptors . K-ATP channel openers and GABA, receptor agonist, per se, had little effect on the postincision allodynic response. The Ca2+ channel blocker of N-type (omega -conotoxin GVIA, 0. 1-3 mu g), but not of P/Q-type (omega-agatoxin IVA), L -type (verapamil, diltiazem or nimodipine), or T-type (mibefradil) , attenuated the incision-induced allodynia, as did gabapentin. Both the antiallodynic effects of gabapentin and omega-conotoxin GVIA were attenuated by Bay K 8644, an L- type Ca2+ channel activator. These results provide correlative evidence to support the contention that N-type Ca2+ channels, but not K-ATP channels or NMDA or GABA(A) receptors, might be involved in the antiallodynic effect of intrathecal gabapentin. |
| Relation: | ANESTHESIA AND ANALGESIA v.102 n.1 pp.182-187 |
| Appears in Collections: | [Dept. of Pharmacology and Graduate Institute of Pharmacology] Periodical Articles
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