ISSN:
1471-4159
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Abstract: The opioid modulation of histamine release was studied in rat brain slices labeled with L-[3H]histidine. The K+-induced [3H]histamine release from cortical slices was progressively inhibited by the preferential k-agonists ketocyclazocine, dynorphin A (1–13), Cambridge 20, spiradoline, U50,488H, and U69,593 in increasing concentrations. In contrast, the μ-agonists morphine, morphiceptin, and Tyr-D-Ala-Gly(NMe)Phe-Gly-ol (DAGO) were ineffective as were the preferential δ-agonists [D-Ala2,D-Leu5]enkephalin (DADLE) and [D-Pen2,D-Pen5]enkephalin (DPDPE). Nor-binaltorphimine (nor-BNI) and MR 2266, two preferential k-antagonists, reversed the inhibitory effect of the various k-agonists more potently than did naloxone, with mean Ki values of 4 nM and 25 nM, respectively. The effects of ketocyclazocine and naloxone also were seen in slices of rat striatum, another brain region known to contain histaminergic nerve endings. We conclude that k-opioid receptors, presumably located on histaminergic axons, control histamine release in the brain. However, nor-BNI and naloxone failed, when added alone, to enhance significantly [3H]histamine release from cerebral cortex or striatum, and bestatin, an aminopeptidase inhibitor, failed to decrease K+-evoked [3H]histamine release. These two findings suggest that under basal conditions these K-opioid receptors are not tonically activated by endogenous dynorphin peptides. The inhibition of cerebral histamine release by K-agonists may mediate the sedative actions of these agents in vivo.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1471-4159.1990.tb08819.x
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