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Spinal antinociception of synthetic omega-conotoxin SO-3, a selective N-type neuronal voltage-sensitive calcium channel blocker, and its effects on morphine analgesia in chemical stimulus tests in rodent.
Eur J Pharmacol. 2010 Jun 25; 636(1-3):73-81.EJ

Abstract

SO-3, a novel Omega-superfamily conotoxin derived from Conus striatus, selectively inhibits N-type neuronal voltage-sensitive calcium channels. In current study, antinociception of SO-3 compared with MVIIA or morphine and its effects on morphine analgesia were investigated in rodent chemical stimulus tests after acute or repeated intrathecal administration. In mice acetic acid writhing test, similar to MVIIA, SO-3 caused dose- and time-dependent spinal antinociception with ED(50) of 0.25 microg/kg and t(1/2) of 4h, which was more potent and longer-acting than morphine. In rat formalin test after intrathecal bolus injection, SO-3 produced dose- and time-dependent antinociception by suppressing acute (ED(50), 1.79 microg/kg) and tonic phases (ED(50), 0.41 microg/kg), which was similar to MVIIA and approximately 10-fold potency and twice longer-acting of morphine in blocking tonic phase responses. After repeated intrathecal injections twice daily for 5 consecutive days, SO-3 produced analgesia without loss of potency whereas morphine produced analgesia tolerance in rat formalin test; further, SO-3 still produced potent analgesia in morphine-tolerant rats. SO-3 co-administered with morphine left-shift the dose-response curve of morphine in mice acetic acid writhing test and significantly potentiated morphine analgesia in rat formalin test. No changes in motor function were seen in mice or rats receiving antinociceptive doses of SO-3 whereas MVIIA caused motor dysfunction at doses of 1.0-2.0 microg/kg in rats. This study showed that (1) novel SO-3 produced potent and long-acting spinal antinociception without observable motor dysfunction, (2) SO-3 significantly potentiated morphine analgesia, (3) After repeated intrathecal administration, SO-3 produced neither tolerance nor cross-tolerance to morphine analgesia.

Authors+Show Affiliations

Beijing Institute of Pharmacology and Toxicology, 27 Tai-Ping Road, Haidian District, Beijing 100850, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20361956

Citation

Yan, Ling-Di, et al. "Spinal Antinociception of Synthetic Omega-conotoxin SO-3, a Selective N-type Neuronal Voltage-sensitive Calcium Channel Blocker, and Its Effects On Morphine Analgesia in Chemical Stimulus Tests in Rodent." European Journal of Pharmacology, vol. 636, no. 1-3, 2010, pp. 73-81.
Yan LD, Liu YL, Zhang L, et al. Spinal antinociception of synthetic omega-conotoxin SO-3, a selective N-type neuronal voltage-sensitive calcium channel blocker, and its effects on morphine analgesia in chemical stimulus tests in rodent. Eur J Pharmacol. 2010;636(1-3):73-81.
Yan, L. D., Liu, Y. L., Zhang, L., Dong, H. J., Zhou, P. L., Su, R. B., Gong, Z. H., & Huang, P. T. (2010). Spinal antinociception of synthetic omega-conotoxin SO-3, a selective N-type neuronal voltage-sensitive calcium channel blocker, and its effects on morphine analgesia in chemical stimulus tests in rodent. European Journal of Pharmacology, 636(1-3), 73-81. https://doi.org/10.1016/j.ejphar.2010.03.036
Yan LD, et al. Spinal Antinociception of Synthetic Omega-conotoxin SO-3, a Selective N-type Neuronal Voltage-sensitive Calcium Channel Blocker, and Its Effects On Morphine Analgesia in Chemical Stimulus Tests in Rodent. Eur J Pharmacol. 2010 Jun 25;636(1-3):73-81. PubMed PMID: 20361956.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Spinal antinociception of synthetic omega-conotoxin SO-3, a selective N-type neuronal voltage-sensitive calcium channel blocker, and its effects on morphine analgesia in chemical stimulus tests in rodent. AU - Yan,Ling-Di, AU - Liu,Yan-Li, AU - Zhang,Lei, AU - Dong,Hua-Jin, AU - Zhou,Pei-Lan, AU - Su,Rui-Bin, AU - Gong,Ze-Hui, AU - Huang,Pei-Tang, Y1 - 2010/03/31/ PY - 2009/11/18/received PY - 2010/02/25/revised PY - 2010/03/12/accepted PY - 2010/4/6/entrez PY - 2010/4/7/pubmed PY - 2010/8/10/medline SP - 73 EP - 81 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 636 IS - 1-3 N2 - SO-3, a novel Omega-superfamily conotoxin derived from Conus striatus, selectively inhibits N-type neuronal voltage-sensitive calcium channels. In current study, antinociception of SO-3 compared with MVIIA or morphine and its effects on morphine analgesia were investigated in rodent chemical stimulus tests after acute or repeated intrathecal administration. In mice acetic acid writhing test, similar to MVIIA, SO-3 caused dose- and time-dependent spinal antinociception with ED(50) of 0.25 microg/kg and t(1/2) of 4h, which was more potent and longer-acting than morphine. In rat formalin test after intrathecal bolus injection, SO-3 produced dose- and time-dependent antinociception by suppressing acute (ED(50), 1.79 microg/kg) and tonic phases (ED(50), 0.41 microg/kg), which was similar to MVIIA and approximately 10-fold potency and twice longer-acting of morphine in blocking tonic phase responses. After repeated intrathecal injections twice daily for 5 consecutive days, SO-3 produced analgesia without loss of potency whereas morphine produced analgesia tolerance in rat formalin test; further, SO-3 still produced potent analgesia in morphine-tolerant rats. SO-3 co-administered with morphine left-shift the dose-response curve of morphine in mice acetic acid writhing test and significantly potentiated morphine analgesia in rat formalin test. No changes in motor function were seen in mice or rats receiving antinociceptive doses of SO-3 whereas MVIIA caused motor dysfunction at doses of 1.0-2.0 microg/kg in rats. This study showed that (1) novel SO-3 produced potent and long-acting spinal antinociception without observable motor dysfunction, (2) SO-3 significantly potentiated morphine analgesia, (3) After repeated intrathecal administration, SO-3 produced neither tolerance nor cross-tolerance to morphine analgesia. SN - 1879-0712 UR - https://www.unboundmedicine.com/medline/citation/20361956/Spinal_antinociception_of_synthetic_omega_conotoxin_SO_3_a_selective_N_type_neuronal_voltage_sensitive_calcium_channel_blocker_and_its_effects_on_morphine_analgesia_in_chemical_stimulus_tests_in_rodent_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-2999(10)00233-5 DB - PRIME DP - Unbound Medicine ER -