Crino P B, Vogt B A, Volicer L, Wiley R G
Department of Behavioral Neurology, Boston University School of Medicine, Massachusetts.
J Pharmacol Exp Ther. 1990 Feb;252(2):651-6.
Experimental lesions followed by binding of [3H]8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), [125I]cyanopindolol and [3H] paroxetine to cryostat sections and coverslip autoradiography were used to localize 5-HT1A, 5-HT1B and 5-HT uptake sites in rat posterior cingulate cortex. Ablations included: 1) undercutting for removal of all afferent axons; 2) destruction of the raphe nuclei; 3) cortical ibotenic acid injections for removal of neurons and 4) anterior thalamic and caudate nuclei injections of the immunotoxin OX7-saporin which destroys single classes of cortical projection neurons by retrograde axonal transport. Peak paroxetine binding was in layer Ia with low binding in layer Va and moderate amounts in other layers. Undercut lesions reduced binding only in layer Ia by 35%. Major loses were observed after raphe ablations with decreases of 40 to 72% across all layers. Cortical ibotenic acid injections did not alter paroxetine binding. Peak cyanopindolol binding was in layers Ia to Ic. Undercutting decreased binding significantly in layers Ia, Ib, III and IV, whereas after raphe lesions binding was decreased by 34 to 58% in layers Ia to IV. 5,7-Dihydroxytryptamine injection increased binding by 10 to 40% in layers Ib, II, III and IV. Cortical ibotenic acid injections reduced grain density in all layers with a range of 28 to 47%. Peak 8-OH-DPAT binding was in layer Vb. No change was observed after undercut lesions, whereas after cortical ibotenic acid injection, binding reductions of 44 to 75% were observed throughout all nine sublaminae. Thalamic OX7-saporin injections destroyed almost all layer VI neurons, which resulted in a 45% decrease in layer VI 8-OH-DPAT binding.(ABSTRACT TRUNCATED AT 250 WORDS)
通过对实验性损伤后的大鼠扣带回后部低温恒温器切片和盖玻片放射自显影进行[3H]8-羟基-2-(二正丙基氨基)四氢萘(8-OH-DPAT)、[125I]氰吲哚洛尔和[3H]帕罗西汀结合实验,来定位5-羟色胺1A(5-HT1A)、5-羟色胺1B(5-HT1B)和5-羟色胺摄取位点。损伤包括:1)切除以去除所有传入轴突;2)损毁中缝核;3)皮质注射鹅膏蕈氨酸以去除神经元;4)丘脑前部和尾状核注射免疫毒素OX7-皂草素,其通过逆行轴突运输破坏单类皮质投射神经元。帕罗西汀结合峰值位于Ia层,Va层结合低,其他层结合量中等。切除损伤仅使Ia层结合减少35%。中缝损毁后观察到主要损失,所有层结合减少40%至72%。皮质注射鹅膏蕈氨酸未改变帕罗西汀结合。氰吲哚洛尔结合峰值位于Ia至Ic层。切除使Ia、Ib、III和IV层结合显著减少,而中缝损伤后,Ia至IV层结合减少34%至58%。注射5,7-二羟基色胺使Ib、II、III和IV层结合增加10%至40%。皮质注射鹅膏蕈氨酸使所有层颗粒密度降低28%至47%。8-OH-DPAT结合峰值位于Vb层。切除损伤后未观察到变化,而皮质注射鹅膏蕈氨酸后,所有九个亚层结合减少44%至75%。丘脑注射OX7-皂草素破坏了几乎所有VI层神经元,导致VI层8-OH-DPAT结合减少45%。(摘要截短于250字)