Zhongguo yao li xue bao = Acta pharmacologica Sinica · 1999
Supraspinal D2 receptor involved in antinociception induced by l-tetrahydropalmatine.
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Hu J Y, Jin G Z
Аннотация
AIM: To study the role of dopamine (DA) receptors in l-tetrahydropalmatine (l-THP)-induced antinociception.
METHODS: The intraperitoneal (i.p.) and intrathecal (ith) injections were used to give the drugs. The tail-flick test was used to assess the nociceptive threshold of rats.
RESULTS: By i.p. injection, l-THP (10, 20, 40 mg.kg-1) as well as D2 receptor antagonist spiperone (1, 2, 3 mg.kg-1) produced dose-dependent antinociceptive effects on the nociception of rats, while D2 receptor agonist quinpirole, D1 receptor agonist SKF38393, and D1 receptor antagonist Sch-23390 showed no antinociception. Moreover, l-THP- or spiperone-induced antinociception was markedly attenuated by quinpirole (2, 3 mg.kg-1) but not SKF38393 or naloxone. On the other hand, ith quinpirole (20, 30, 40 micrograms.kg-1) also induced a dose-dependent antinociception, while ith l-THP, spiperone, SKF38393, and Sch-23390 did not exhibit any antinociception. Furthermore, ith spiperone (20, 30, 40 micrograms.kg-1) but not Sch-23390 dose-dependently antagonised the antinociception induced by quinpirole. l-THP (ith, 100, 200, 300 micrograms.kg-1) also dramatically attenuated the quinpirole-induced antinociception with a dose-dependent relationship.
CONCLUSION: Activating the spinal D2 receptor or blocking the supraspinal D2 receptor produces antinociception. D1 receptor might be not directly involved in the antinociception. l-THP (as a D2 antagonist) as well as spiperone produces antinociception via blocking the supraspinal D2 receptor.
METHODS: The intraperitoneal (i.p.) and intrathecal (ith) injections were used to give the drugs. The tail-flick test was used to assess the nociceptive threshold of rats.
RESULTS: By i.p. injection, l-THP (10, 20, 40 mg.kg-1) as well as D2 receptor antagonist spiperone (1, 2, 3 mg.kg-1) produced dose-dependent antinociceptive effects on the nociception of rats, while D2 receptor agonist quinpirole, D1 receptor agonist SKF38393, and D1 receptor antagonist Sch-23390 showed no antinociception. Moreover, l-THP- or spiperone-induced antinociception was markedly attenuated by quinpirole (2, 3 mg.kg-1) but not SKF38393 or naloxone. On the other hand, ith quinpirole (20, 30, 40 micrograms.kg-1) also induced a dose-dependent antinociception, while ith l-THP, spiperone, SKF38393, and Sch-23390 did not exhibit any antinociception. Furthermore, ith spiperone (20, 30, 40 micrograms.kg-1) but not Sch-23390 dose-dependently antagonised the antinociception induced by quinpirole. l-THP (ith, 100, 200, 300 micrograms.kg-1) also dramatically attenuated the quinpirole-induced antinociception with a dose-dependent relationship.
CONCLUSION: Activating the spinal D2 receptor or blocking the supraspinal D2 receptor produces antinociception. D1 receptor might be not directly involved in the antinociception. l-THP (as a D2 antagonist) as well as spiperone produces antinociception via blocking the supraspinal D2 receptor.