Evidence map›Paper›PMID 25337379›Full record

ArticleBasic and clinical neuroscience2014

ATP-sensitive Potassium Channels and L-type Calcium Channels are Involved in Morphine-induced Hyperalgesia after Nociceptive Sensitization in Mice.

Shamseddin Ahmadi, Shaho Azarian, Sayede Shohre Ebrahimi, Ameneh Rezayof

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Article in Basic and clinical neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
0.5field-weighted citation impact, top 34% of its field
1 · What the graph read from it

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3 · Its place in the literature

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0 citing papers in PubMed, 4 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Shamseddin AhmadiDepartment of Biological Science and Biotechnology, Faculty of Science, University of Kurdistan, Sanandaj, Iran.
Shaho AzarianDepartment of Animal Biology, School of Biology, University college of Science, University of Tehran, Tehran, Iran.
Sayede Shohre EbrahimiDepartment of Biological Science and Biotechnology, Faculty of Science, University of Kurdistan, Sanandaj, Iran.
Ameneh RezayofDepartment of Animal Biology, School of Biology, University college of Science, University of Tehran, Tehran, Iran.
University of Kurdistan · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionWe investigated the role of ATP-sensitive potassium channels and L-type calcium channels in morphine-induced hyperalgesia after nociceptive sensitization.

methodsWe used a hotplate apparatus to assess pain behavior in male NMRI mice. Nociceptive sensitization was induced by three days injection of morphine and five days of drug free. On day 9 of the schedule, pain behavior test was performed for evaluating the effects of morphine by itself and along with nimodipine, a blocker of L-type calcium channels and diazoxide, an opener of ATP-sensitive potassium channels. All drugs were injected through an intraperitoneal route.

resultsThe results showed that morphine (7.5, 10 and 15 mg/kg) induced analgesia in normal mice, which was prevented by naloxone (1 mg/kg). After nociceptive sensitization, analgesic effect of morphine (10 and 15 mg/kg) was significantly decreased in sensitized mice. The results showed that nimodipine (2.5, 5, 10 and 20 mg/kg) had no significant effect on pain behavior test in either normal or sensitized mice. However, nimodipine (20 mg/ kg) along with morphine (10 and 15 mg/kg) caused more decrease in morphine analgesia in sensitized mice. Furthermore, diazoxide by itself (0.25, 1, 5 and 20 mg/kg) had also no significant effect on pain behavior in both normal and sensitized mice, but at dose of 20 mg/kg along with morphine (10 and 15 mg/kg) decreased analgesic effect of morphine in sensitized mice. DISCUSSION: It can be concluded that potassium and calcium channels have some roles in decrease of analgesic effect of morphine after nociceptive sensitization induced by pretreatment of morphine.

Indexed as

DiazoxideMorphineNimodipinePain BehaviorSensitization

Identifiers

PMID25337379
PMCPMC4202544
OpenAlexW1898749679

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