Modulation of retinotectal transmission by presynaptic 5-HT1B receptors in the superior colliculus of the adult hamster.
Modulation of retinotectal transmission by presynaptic 5-HT1B receptors in the superior colliculus of the adult hamster.
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成年仓鼠上丘突触前 5-HT1B 受体对视网膜顶盖传输的调节。
DOI：
10.1152/jn.1994.72.1.3
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发表时间：
1994
影响因子：
2.5
通讯作者：
Rhoades,RW
中科院分区：
文献类型：
--
作者：
Mooney,RD;Shi,MY;Rhoades,RW
1.用放射性配体与异丙肾上腺素存在下的[125 I] -氰基吲哚酚结合来确定5 -HT 1B受体在成年仓鼠上级丘（SC）中的分布。这些受体在表层灰层（SGS）中密度较高，而在SC的其他层中密度较低。摘除一只眼睛产生了显着的减少，这些受体的密度在对侧SGS，这表明它们主要位于视网膜顶盖轴突终端。2.应用细胞内记录技术，观察了5-羟色胺（5 -HT）对刺激视束（OT）诱发的成年仓鼠SC细胞兴奋性突触后电位（EPSP）的影响。应用5 -HT在测试的67个细胞中的79%中产生了>或= 50%的OT诱发的EPSP的减少。对照组平均EPSP振幅为7.8 ± 2.1（SD）mV，5 -HT组为2.7 ± 1.9 mV（P < 0.01）。对于大多数这些神经元，应用5 -HT对其膜电位或输入电阻的影响不大。用5 -HT测试的细胞膜电位的平均百分比变化为0.5 +/- 6.0%，输入电阻的平均百分比变化为0.6 +/-22.9%。3.对于四个测试的六个细胞，应用5 -HT没有显着的影响，应用谷氨酸引起的反应，无论是在正常的洗澡条件下，或当介质包括低Ca 2+和高Mg 2+。4.药理实验表明，5 -HT对视网膜顶盖传递的作用可被5 -HT 1B激动剂1 -[3 -（三氟甲基）苯基] -哌嗪和7 -三氟甲基-4-（4-甲基-1 -哌嗪基）[1，2-a] -喹喔啉马来酸盐所模拟，并被5 -HT 1A/1B拮抗剂（-）-吲哚洛尔和甲硫替平所拮抗。螺哌隆、酮色林、1 -（2 -甲氧基苯基）-4 -[4 -（2 -邻苯二甲酰亚胺基）丁基] -哌嗪HBr或[1 -H-3 α-5 α-托烷-3 -基]-3，5-二氯苯甲酸酯均不能拮抗5 -HT对OT诱发的EPSP的作用。5.解剖学和生理学结果均与5 -HT突触前抑制视网膜顶盖传递的结论一致，并且这种作用是由5 -HT 1B受体介导的
1. Radioligand binding with [125I] -cyanopindolol in the presence of isoproterenol was used to define the distribution of 5 -HT1B receptors in the superior colliculus (SC) of adult hamsters. There was a high density of these receptors in the stratum griseum superficiale (SGS), and they were much less dense in other SC laminae. Enucleation of one eye produced a marked reduction in the density of these receptors in the contralateral SGS, suggesting that they are located primarily on retinotectal axon terminals. 2. Intracellular recording techniques were used to evaluate the effects of serotonin (5 -HT) on the excitatory postsynaptic potentials (EPSPs) evoked in SC cells of adult hamsters by stimulation of the optic tract (OT) in vitro. Application of 5 -HT produced a reduction of > or = 50% in OT -evoked EPSPs in 79% of the 67 cells tested. The average EPSP amplitude was 7.8 +/- 2.1 (SD) mV under control conditions and 2.7 +/- 1.9 mV in the presence of 5 -HT (P < 0.01). For most of these neurons, application of 5 -HT had little effect on their membrane potential or input resistance. The average percent change in membrane potential for cells tested with 5 -HT was 0.5 +/- 6.0% and the average percent change in input resistance was 0.6 +/- 22.9%. 3. For four of six cells tested, application of 5 -HT had no significant effects on the responses evoked by application of glutamate, either under normal bathing conditions or when the medium included low Ca2+ and high Mg2+. 4. Pharmacologic experiments indicated that the effects of 5 -HT on retinotectal transmission were mimicked by the 5 -HT1B agonists 1 -[3 -(trifluoromethyl)phenyl] -piperazine and 7 -trifluoromethyl -4(4 -methyl -1 -piperazinyl) [1,2 -a] -quinoxaline maleate and antagonized by the 5 -HT1A/1B antagonists ( -) -pindolol and methiothepin. The effects of 5 -HT on the OT -evoked EPSP were not antagonized by either spiperone, ketanserin, 1 -(2 -methoxyphenyl) -4 -[4 -(2 -phthalimido)butyl] -piperazine HBr, or [1 -H -3 alpha -5 alpha -tropan -3 -yl] -3,5 -dichlorobenzoate. 5. Both the anatomic and physiological results are consistent with the conclusion that 5 -HT presynaptically inhibits retinotectal transmission and that this effect is mediated by the 5 -HT1B receptor