幼年大鼠皮质5—HT_(1A)和5—HT_2受体中介的膜电位变化  

5-HT_1A, AND 5-HT_2 RECEPTORS MEDIATE MEMBRANE POTENTIAL CHANGES IN NEONATE RAT CORTEX

作　　者：史明仪[1] 陈琦[1] 周华珠[1] 

机构地区：[1]扬州医学院生理教研室

出　　处：《神经科学》1995年第3期127-130,共4页Chinese Journal of Neuroscience

摘　　要：５—ＨＴ灌流幼年大鼠皮质脑片，２１５的额叶后部Ⅳ层神经元出现慢超极化、膜电阻减小和ＥＰＳＰ抑制。此效应为５—ＨＴ_１Ａ激动剂８—ＯＨ—ＤＰＡＴ模拟；为５—ＨＴ１Ａ拮抗剂ＮＡＮ—１９０阻抑，但ＥＰＳＰ抑制仍存在；超极化幅度随膜电位增大及胞外钾浓度增高而减少，表明超极化由激活５—ＨＴ１Ａ受体导致钾外流增加所致。另有１１．８％神经元出现去极化伴膜电阻减小和ＥＰＳＰ抑制，５—ＨＴ_５／５—ＨＴ１ｃ拮抗剂Ｋｅｔａｎｓｅｒｉｎ阻抑前两种效应，提示去极化与５—ＨＴ２受体及钾外流减少有关。上述结果也表明ＥＰＳＰ抑制主要不是由５—ＨＴ１Ａ和５—ＴＨ２受体中介，与膜电位变化为相互独立的过程。We have studied the 5-HT receptors in postfrontalis cortex by intracellular and whole cell Patch recording in brain slices cut obliquely in order to Preserve the thalamo-cortical projection. Bath application of 5-HT invariably reduced the amplitude of evoked EPSP's, which was companied by a slow hyperpolarization and a decrease in input resistance in 21.5% of cells tested. The hyperpolarization was mimicked by 5-HT_1A agonist 8-OH-DPAT and blocked by 5-HT_1A, antagonist NAN-190 while the inhibition of EPSPs still existed.The amplitude of the hyperpolarization, persisting in a low Ca2+ high Mg2+ solution, was reduced 6y elevated [K+]. It appears that 5-HT directly acts on 5-HT_1A, receptor and hyperpolarizes the neurons by increasing K+ conductance.A slow depolarization with an increase in input resistance and an inhibition of EPSPs, blocked by 5-HT_2,/5-HT_c. antagonist Ketanserin, was induced in other 11.8% of the neurons tested. It suggests that 5-HT probably acts on 5-HT_2 receptor and depolarizes the neurons by decreasing K+ conductance.The inhibition of EPSPs was independent of the membrane potential changes and mediatsd mainly by 5-HT_18 receptor presynaptially.

关 键 词：超极化 去极化 皮质 5-羟色胺 

分 类 号：R338.2[医药卫生—人体生理学] R338.8[医药卫生—基础医学]