Nicotine blocks apomorphine‐induced disruption of prepulse inhibition of the acoustic startle in rats: possible involvement of central nicotinic α7 receptors

Nicotine blocks apomorphine‐induced disruption of prepulse inhibition of the acoustic startle in rats: possible involvement of central nicotinic α7 receptors
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尼古丁阻断阿朴吗啡诱导的大鼠声惊吓前脉冲抑制的破坏:可能涉及中枢烟碱α7受体

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发表时间:
2004
影响因子:
7.3
通讯作者:
Y. Gomita
Y. Gomita
中科院分区:
医学2区
文献类型:
--
作者:
K. Suemaru;K. Yasuda;Kenta Umeda;H. Araki;K. Shibata;T. Choshi;S. Hibino;Y. Gomita

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据报道,尼古丁可以使精神分裂症患者的听觉门控缺陷正常化,这表明尼古丁乙酰胆碱受体参与了注意异常。然而,其机制仍不清楚。本研究观察了尼古丁对阿朴吗啡或苯环利定诱导的大鼠声惊厥反应的脉冲前抑制(PPI)的影响。在测试的剂量范围内,尼古丁(0.05-1 mg kg−1,S.C.)没有扰乱PPI。α7烟碱受体拮抗剂甲基乌头碱(0.5~5 mg kgβ1,s.c)和−4α2烟碱受体拮抗剂二氢β红碱(0.5~2 mg kg−1,s.c)对PPI均无影响。尼古丁(0.01-0.2mgkg−1,S.C.)阿朴吗啡(1 mg kg−-1,sc)可剂量依赖性地逆转阿朴吗啡(1 mg kg−-1,sc)对PPI的干扰作用,但对苯环利定(2 mg kg-1,sc)所致PPI的干扰无明显影响。烟碱(0.2mgkg−-1)逆转阿朴吗啡引起的PPI值的改变可被甲乙胺(1 mg kg−-1,i.p)所阻断,但不能被六甲基溴铵(10 mg kg-−-1,i.p)所阻断,表明中枢烟碱受体参与了这一过程。尼古丁对阿朴吗啡引起的PPI破坏的拮抗作用可被甲基琥珀酸碱(1和2 mg kg−-1,S.C.)剂量依赖地阻断。而二氢-β-红景天碱(1和2 mg kg−1,S.C.)没有任何效果。这些结果表明,尼古丁通过中枢α7烟碱受体逆转阿朴吗啡诱导的PPI的破坏。
Nicotine has been reported to normalize deficits in auditory sensory gating in the cases of schizophrenia, suggesting an involvement of nicotinic acetylcholine receptors in attentional abnormalities. However, the mechanism remains unclear. The present study investigated the effects of nicotine on the disruption of prepulse inhibition (PPI) of the acoustic startle response induced by apomorphine or phencyclidine in rats. Over the dose range tested, nicotine (0.05–1 mg kg−1, s.c.) did not disrupt PPI. Neither methyllycaconitine (0.5–5 mg kg−1, s.c.), an α7 nicotinic receptor antagonist, nor dihydro‐β‐erythroidine (0.5–2 mg kg−1, s.c.), an α4β2 nicotinic receptor antagonist, had any effect on PPI. Nicotine (0.01–0.2 mg kg−1, s.c.) dose‐dependently reversed the disruption of PPI induced by apomorphine (1 mg kg−1, s.c.), but had no effect on the disruption of PPI induced by phencyclidine (2 mg kg−1, s.c.). The reversal of apomorphine‐induced PPI disruption by nicotine (0.2 mg kg−1) was eliminated by mecamylamine (1 mg kg−1, i.p.), but not by hexamethonium (10 mg kg−1, i.p.), indicating the involvement of central nicotinic receptors. The antagonistic action of nicotine on apomorphine‐induced PPI disruption was dose‐dependently blocked by methyllycaconitine (1 and 2 mg kg−1, s.c.). However, dihydro‐β‐erythroidine (1 and 2 mg kg−1, s.c.) had no effect. These results suggest that nicotine reverses the disruption of apomorphine‐induced PPI through central α7 nicotinic receptors.
DOI: 10.1093/schbul/23.2.247
发表时间: 1997
影响因子: 6.6
作者:
D. Ziedonis;T. George
通讯作者: D. Ziedonis;T. George
DOI: 10.1001/archpsyc.1990.01810140081011
发表时间: 1990-02
影响因子: --
作者:
D. Braff;M. Geyer
通讯作者: D. Braff;M. Geyer
DOI: 10.1126/science.7569895
发表时间: 1995-09-22
期刊: SCIENCE
影响因子: 56.9
作者:
MCGEHEE, DS;HEATH, MJS;ROLE, LW
通讯作者: ROLE, LW
DOI: --
发表时间: 1994-11
期刊: The Journal of pharmacology and experimental therapeutics
影响因子: --
作者:
V. Bakshi;N. Swerdlow;M. Geyer
通讯作者: V. Bakshi;N. Swerdlow;M. Geyer
DOI: --
发表时间: 1990
期刊: Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
影响因子: --
作者:
Peng,RY;Mansbach,RS;Braff,DL;Geyer,MA
通讯作者: Geyer,MA