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大鼠腹侧被盖区中5-羟色胺与多巴胺的相互作用:一项体内电生理研究

Serotonin-dopamine interaction in the rat ventral tegmental area: an electrophysiological study in vivo.

作者信息

Prisco S, Pagannone S, Esposito E

机构信息

Istituto di Ricerche Farmacologiche Mario Negri, Chieti, Italy.

出版信息

J Pharmacol Exp Ther. 1994 Oct;271(1):83-90.

PMID:7965760
Abstract

Electrophysiological techniques were used to study the effects of various serotonin (5-HT) agonists and antagonists on the activity of dopamine (DA) neurons in the ventral tegmental area (VTA) of rats. Systemic administration of the selective 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) (1.25-80 micrograms/kg i.v.) increased the firing rate of the majority (75%) of DA cells studied and stimulated their bursting activity. A subpopulation (25%) of DA neurons was inhibited by 8-OH-DPAT. Selective lesions of 5-HT neurons by the neurotoxin 5-7-dihydroxytryptamine abolished completely the excitatory effect of 8-OH-DPAT on both firing rate and bursting activity of DA neurons. Microiontophoretic application of 8-OH-DPAT into the VTA did not cause any change in the firing rate of DA neurons. Treatment with the selective 5-HT1B agonist CGS 12066B (7-trifluoromethyl-4-(4-methyl-1-piperazinyl)-pyrolo[1,2-a] quinoxaline 1:2 maleate salt) (1.25-160 micrograms/kg i.v.) did not cause any change in basal firing rate of VTA DA cells. Systemic administration of trifluoromethylphenylpiperazine (TFMPP) (1.25-160 micrograms/kg i.v.) and m-chlorophenylpiperazine (mCPP) (1.25-320 micrograms/kg i.v.), two mixed 5-HT1B/5-HT1C receptor agonists, significantly reduced the firing rate of all VTA DA neurons studied. The effect of mCPP (maximal inhibition, 40%) was more pronounced compared to that of TFMPP (maximal inhibition, 25%). Microiontophoretic application of mCPP into the VTA caused a marked inhibition of the basal activity of DA neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

采用电生理技术研究了各种血清素(5-羟色胺,5-HT)激动剂和拮抗剂对大鼠腹侧被盖区(VTA)多巴胺(DA)神经元活性的影响。选择性5-HT1A受体激动剂8-羟基-2-(二正丙基氨基)四氢萘(8-OH-DPAT)(静脉注射1.25 - 80微克/千克)可使所研究的大多数(75%)DA细胞的放电频率增加,并刺激其爆发性活动。一小部分(25%)DA神经元受到8-OH-DPAT的抑制。用神经毒素5,7-二羟基色胺对5-HT神经元进行选择性损伤,可完全消除8-OH-DPAT对DA神经元放电频率和爆发性活动的兴奋作用。将8-OH-DPAT微量离子导入VTA不会引起DA神经元放电频率的任何变化。用选择性5-HT1B激动剂CGS 12066B(7-三氟甲基-4-(4-甲基-1-哌嗪基)-吡咯并[1,2-a]喹喔啉1:2马来酸盐)(静脉注射1.25 - 160微克/千克)处理,不会引起VTA DA细胞基础放电频率的任何变化。两种5-HT1B/5-HT1C混合受体激动剂三氟甲基苯基哌嗪(TFMPP)(静脉注射1.25 - 160微克/千克)和间氯苯基哌嗪(mCPP)(静脉注射1.25 - 320微克/千克)全身给药,可显著降低所研究的所有VTA DA神经元的放电频率。与TFMPP(最大抑制率25%)相比,mCPP的作用(最大抑制率40%)更明显。将mCPP微量离子导入VTA可显著抑制DA神经元的基础活性。(摘要截于250字)

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