Effects of 5-HT on thalamocortical synaptic transmission in the developing rat.
Effects of 5-HT on thalamocortical synaptic transmission in the developing rat.
复制标题
DOI：
10.1152/jn.1994.72.5.2438
复制
发表时间：
1994-11
影响因子：
2.5
通讯作者：
Robert W. Rhoades;C. Bennett-Clarke;Ming-Yi Shi;Richard D. Mooney
中科院分区：
文献类型：
--
作者：
Robert W. Rhoades;C. Bennett-Clarke;Ming-Yi Shi;Richard D. Mooney
1.最近的免疫细胞化学和受体结合的数据表明，一个短暂的躯体定位图案的5-羟色胺（5-HT）的免疫反应纤维在初级体感皮层的发育大鼠和5-HT 1B受体的丘脑皮质轴突的腹后内侧丘脑核（VPM）的短暂表达。2.这些结果表明，5-HT强烈调节丘脑皮层突触传递有限的时间在出生后的发展。这一假设进行了测试，在丘脑皮层切片制备，包括VPM，丘脑辐射，和初级躯体感觉皮层的细胞内记录实验。监测5-HT及其类似物对皮层神经元膜电位和输入电阻以及刺激VPM诱发的突触电位振幅的影响。3.结果表明，5-HT能强烈抑制VPM诱发的兴奋性突触后电位（EPSP），并呈剂量依赖性。与此相反，5-HT没有显着的影响膜电位，输入电阻，或去极化诱导谷氨酸直接应用于皮层细胞。4. 5-HT_（1B）受体激动剂1-[3-（三氟甲基）苯基]-哌嗪（TFMPP）和7-三氟甲基-4-（4-甲基-1-哌嗪基）-吡咯并[1，2-a]-喹喔啉马来酸盐可模拟5-HT的作用，而5-HT_（1B）受体拮抗剂（-）-吲哚洛尔可拮抗5-HT的作用。5-HT 1A激动剂[（+/-）8-羟基二丙氨基四氢萘HBr]（8-OH-DPAT）对VPM诱发的EPSP的作用较小，而5-HT对这种反应的作用一般不被1-（2-甲氧基苯基）-4-[4-（2-邻苯二甲酰亚胺基）丁基]哌嗪HBr（一种5-HT 1A拮抗剂）或酮丝氨酸（一种5-HT 2拮抗剂）或螺哌隆（一种5-HT 1A和2拮抗剂）拮抗。5. 5-HT抑制VPM诱发的皮层神经元EPSP的能力在> 2周龄的动物脑片中显著降低。TFMPP在这些动物中的有效性甚至比5-HT的有效性更弱，而8-OH-DPAT的有效性随着年龄的增长而不变。这些结果与出生后第二周后丘脑皮质轴突上5-HT 1B受体的消失和某些神经元上5-HT 1A受体的维持是一致的。6.所有的结果在这项研究中得到的结论是一致的，5-HT有一个深刻的，但发育短暂的，突触前抑制作用对丘脑皮层的传递在大鼠的体感皮层。
1. Recent immunocytochemical and receptor binding data have demonstrated a transient somatotopic patterning of serotonin (5-HT)-immunoreactive fibers in the primary somatosensory cortex of developing rats and a transient expression of 5-HT1B receptors on thalamocortical axons from the ventral posteromedial thalamic nucleus (VPM). 2. These results suggest that 5-HT should strongly modulate thalamocortical synaptic transmission for a limited time during postnatal development. This hypothesis was tested in intracellular recording experiments carried out in thalamocortical slice preparations that included VPM, the thalamic radiations, and the primary somatosensory cortex. Effects of 5-HT and analogues were monitored on membrane potentials and input resistances of cortical neurons and on the amplitude of the synaptic potentials evoked in them by stimulation of VPM. 3. Results obtained from cortical neurons in slices taken from rats during the first 2 wk of life indicated that 5-HT strongly inhibited the VPM-evoked excitatory postsynaptic potential (EPSP) recorded from cortical neurons in a dose-dependent manner. In contrast, 5-HT had no significant effects on membrane potential, input resistance, or depolarizations induced by direct application of glutamic acid to cortical cells. 4. The effects of 5-HT were mimicked by the 5-HT1B receptor agonists 1-[3-(trifluoromethyl)phenyl]-piperazine (TFMPP) and 7-trifluoromethyl-4(4-methyl-1-piperazinyl)-pyrrolo[1,2-a]-quinoxaline maleate and antagonized by the 5-HT1B receptor antagonist (-)-pindolol. The 5-HT1A agonist [(+/-)8-hydroxydipropylaminotetralin HBr] (8-OH-DPAT) had less effect on the VPM-elicited EPSP, and the effects of 5-HT upon this response were generally not antagonized by either 1-(2-methoxyphenyl)-4-[4-(2- phthalimmido)butyl]piperazine HBr (a 5-HT1A antagonist) or ketanserine (a 5-HT2 antagonist) or spiperone (a 5-HT1A and 2 antagonist). 5. The ability of 5-HT to inhibit the VPM-evoked EPSP in cortical neurons was significantly reduced in slices from animals > 2 wk of age. The effectiveness of TFMPP in such animals was even more attenuated than that of 5-HT, and the effectiveness of 8-OH-DPAT was unchanged with age. These results are consistent with the disappearance of 5-HT1B receptors from thalamocortical axons after the second postnatal week and the maintenance of 5-HT1A receptors on some neurons. 6. All of the results obtained in this study are consistent with the conclusion that 5-HT has a profound, but developmentally transient, presynaptic inhibitory effect upon thalamocortical transmission in the rat's somatosensory cortex.