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1
Cholecystokinin potentiates dopamine-mediated behaviors: evidence for modulation specific to a site of coexistence.胆囊收缩素增强多巴胺介导的行为:共存位点特异性调节的证据。
J Neurosci. 1985 Aug;5(8):1972-83. doi: 10.1523/JNEUROSCI.05-08-01972.1985.
2
Behavioral evidence for cholecystokinin modulation of dopamine in the mesolimbic pathway.胆囊收缩素对中脑边缘通路多巴胺调节作用的行为学证据。
Prog Clin Biol Res. 1985;192:131-8.
3
Subtype-selective cholecystokinin receptor antagonists block cholecystokinin modulation of dopamine-mediated behaviors in the rat mesolimbic pathway.亚型选择性胆囊收缩素受体拮抗剂可阻断胆囊收缩素对大鼠中脑边缘通路中多巴胺介导行为的调节作用。
J Neurosci. 1992 Sep;12(9):3380-91. doi: 10.1523/JNEUROSCI.12-09-03380.1992.
4
Antagonists of central and peripheral behavioral actions of cholecystokinin octapeptide.胆囊收缩素八肽中枢和外周行为作用的拮抗剂。
J Pharmacol Exp Ther. 1986 Feb;236(2):320-30.
5
Behavioral and neurophysiological evidence for a facilatory interaction between co-existing transmitters: cholecystokinin and dopamine.
Neurochem Int. 1984;6(6):755-60. doi: 10.1016/0197-0186(84)90007-x.
6
Topographical analysis of nucleus accumbens sites at which cholecystokinin potentiates dopamine-induced hyperlocomotion in the rat.
Brain Res. 1985 Jun 3;335(2):337-41. doi: 10.1016/0006-8993(85)90489-5.
7
Cholecystokinin potentiation of dopamine-mediated behaviors in the nucleus accumbens.胆囊收缩素对伏隔核中多巴胺介导行为的增强作用。
Ann N Y Acad Sci. 1985;448:283-92. doi: 10.1111/j.1749-6632.1985.tb29924.x.
8
Opposite actions of CCK-8 on amphetamine-induced hyperlocomotion and stereotypy following intracerebroventricular and intra-accumbens injections in rats.大鼠脑室内和伏隔核内注射后,胆囊收缩素八肽(CCK-8)对苯丙胺诱导的运动亢进和刻板行为的相反作用。
Pharmacol Biochem Behav. 1988 Jun;30(2):309-17. doi: 10.1016/0091-3057(88)90460-1.
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Effect of injection of CCK-8 into the nucleus caudatus on the behavior of rats.向大鼠尾状核注射CCK-8对其行为的影响。
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10
Reversal by cholecystokinin of apomorphine-induced inhibition of dopamine release in the nucleus accumbens of the rat.胆囊收缩素对阿扑吗啡诱导的大鼠伏隔核多巴胺释放抑制的逆转作用。
Regul Pept. 1987 Jun;17(6):301-10. doi: 10.1016/0167-0115(87)90053-x.

引用本文的文献

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Cholecystokinin and psychiatric disorders : role in aetiology and potential of receptor antagonists in therapy.胆囊收缩素与精神障碍:在发病机制中的作用及受体拮抗剂的治疗潜力。
CNS Drugs. 1997 Aug;8(2):134-52. doi: 10.2165/00023210-199708020-00005.
2
Sexual behavior induction of c-Fos in the nucleus accumbens and amphetamine-stimulated locomotor activity are sensitized by previous sexual experience in female Syrian hamsters.在雌性叙利亚仓鼠中,伏隔核中c-Fos的性行为诱导以及苯丙胺刺激的运动活动会因先前的性经验而变得敏感。
J Neurosci. 2001 Mar 15;21(6):2123-30. doi: 10.1523/JNEUROSCI.21-06-02123.2001.
3
Total synthesis, purification, and characterization of human [Phe(p-CH2SO 3Na)52, Nle32,53,56, Nal55]-CCK20-58, [Tyr52, Nle32,53,56, Nal55]-CCK-58, and [Phe(p-CH2SO3Na)52, Nle32,53,56, Nal55]-CCK-58.
J Protein Chem. 1993 Oct;12(5):533-44. doi: 10.1007/BF01025118.
4
The stimulation of cholecystokinin receptors in the rostral nucleus accumbens significantly antagonizes the EEG and behavioural effects induced by phencyclidine in rats.刺激大鼠伏隔核嘴侧的胆囊收缩素受体可显著拮抗苯环利定诱导的脑电图和行为效应。
Psychopharmacology (Berl). 1995 Jul;120(2):156-61. doi: 10.1007/BF02246188.
5
Neurotensin and cholecystokinin coexistence within neurons of the ventral mesencephalon: projections to forebrain.神经降压素与胆囊收缩素在中脑腹侧神经元内共存:向 forebrain 的投射。 (注:这里“forebrain”常见释义为“前脑” ,但在医学专业文献中,有时会使用更宽泛、更符合语境的译法,比如“端脑”等,这里按照常规翻译为“前脑” 。)
Exp Brain Res. 1987;68(2):277-89. doi: 10.1007/BF00248793.
6
Differential effects of proglumide on mesolimbic and nigrostriatal dopamine function.
Psychopharmacology (Berl). 1987;91(4):440-4. doi: 10.1007/BF00216008.
7
CCK-8 injected into the nucleus accumbens attenuates the supersensitive locomotor response to apomorphine in 6-OHDA and chronic-neuroleptic treated rats.向伏隔核注射CCK-8可减弱6-OHDA和慢性抗精神病药物处理大鼠对阿扑吗啡的超敏运动反应。
Psychopharmacology (Berl). 1989;99(3):409-15. doi: 10.1007/BF00445568.
8
Cholecystokinin and tyrosine hydroxylase messenger RNAs in neurons of rat mesencephalon: peptide/monoamine coexistence studies using in situ hybridization combined with immunocytochemistry.大鼠中脑神经元中的胆囊收缩素和酪氨酸羟化酶信使核糖核酸:采用原位杂交与免疫细胞化学相结合的肽/单胺共存研究
Exp Brain Res. 1989;74(1):149-62. doi: 10.1007/BF00248288.
9
Galanin antagonizes acetylcholine on a memory task in basal forebrain-lesioned rats.甘丙肽在基底前脑损伤大鼠的记忆任务中拮抗乙酰胆碱。
Proc Natl Acad Sci U S A. 1988 Dec;85(24):9841-5. doi: 10.1073/pnas.85.24.9841.
10
Tyrosine hydroxylase and cholecystokinin mRNA levels in the substantia nigra, ventral tegmental area, and locus ceruleus are unaffected by acute and chronic haloperidol administration.急性和慢性给予氟哌啶醇对黑质、腹侧被盖区及蓝斑中酪氨酸羟化酶和胆囊收缩素的信使核糖核酸水平无影响。
Cell Mol Neurobiol. 1990 Mar;10(1):41-50. doi: 10.1007/BF00733634.

胆囊收缩素增强多巴胺介导的行为:共存位点特异性调节的证据。

Cholecystokinin potentiates dopamine-mediated behaviors: evidence for modulation specific to a site of coexistence.

作者信息

Crawley J N, Stivers J A, Blumstein L K, Paul S M

出版信息

J Neurosci. 1985 Aug;5(8):1972-83. doi: 10.1523/JNEUROSCI.05-08-01972.1985.

DOI:10.1523/JNEUROSCI.05-08-01972.1985
PMID:4040554
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6565292/
Abstract

Cholecystokinin coexists with dopamine in mesolimbic neurons in mammalian brain. When injected directly into the nucleus accumbens, cholecystokinin (CCK) potentiated dopamine (DA)-induced hyperlocomotion and apomorphine-induced stereotypy. These effects were not mimicked by nonsulfated CCK, but were blocked by proglumide, a putative CCK antagonist, as well as by antisera raised against sulfated CCK. CCK alone had no effect on locomotion or sterotypy, indicating that this peptide acts primarily as a modulator of DA-mediated behaviors in the mesolimbic pathway. In addition, CCK did not potentiate DA-induced hyperlocomotion or apomorphine-induced stereotypy when injected into the caudate nucleus, where CCK and DA are localized in separate neurons in rats. Facilitation of DA-mediated behaviors by CCK may represent a functional interaction specific to the neuromodulator-neurotransmitter coexistence phenomenon.

摘要

胆囊收缩素与多巴胺在哺乳动物脑内的中脑边缘神经元中共存。当直接注射到伏隔核时,胆囊收缩素(CCK)增强多巴胺(DA)诱导的运动亢进和阿扑吗啡诱导的刻板行为。这些作用不能被非硫酸化的CCK模拟,但可被一种假定的CCK拮抗剂丙谷胺以及抗硫酸化CCK的抗血清所阻断。单独的CCK对运动或刻板行为没有影响,表明该肽主要作为中脑边缘通路中DA介导行为的调节剂。此外,当注射到尾状核时,CCK不会增强DA诱导的运动亢进或阿扑吗啡诱导的刻板行为,在大鼠中CCK和DA定位于不同的神经元。CCK对DA介导行为的促进作用可能代表了神经调质 - 神经递质共存现象所特有的功能相互作用。