大鼠嗅球乙酰胆碱酯酶阳性传入纤维起源的实验研究

本文应用荧光素逆行标记与乙酰胆碱酯酶(AchE)组织化学相结合技术,探索了嗅球AchE阳性传入纤维的起源。经观察在注射区同侧的下列核(区)可发现荧酶双标记细胞:嗅前核后部、斜角带核、屏状核、中缝背核、中央上核和蓝斑。     

猫中缝核向嗅球的投射——HRP法研究

本研究用HRP逆轴突传递法观察了猫脑干中缝各核向嗅球的上行投射。实验证明,将HRP注入一侧嗅球后,标记细胞规律性地出现在上位脑干的各中缝核中,即中缝背核(RD)、中央上核(CS)、中间线形核(LI)和吻侧线形核(LR);下位脑干的中缝各核(中缝隐核、中缝苍白核,中缝大核和中缝桥核)全无标记。四个核中出现的标记细胞数各不相同,细胞的分布各有特点。RD中的标记细胞数是四个核中最多的,它们沿中线排列,主要集中于核的中、吻段,尾段极少。CS内的标记细胞数占第二位,仅见于核的尾段,吻段无标记。LI中的标记细胞最少,分散在核的全长。LR中的标记细胞不多,主要出现在同侧核的腹侧部。本研究支持文献中关于RD和CS与嗅球的上行联系的报导,证明了尚未见报导的LI和LR是嗅球传入纤维的另外来源。     

大鼠苍白球乙酰胆碱酯酶阳性纤维起源的实验研究

应用荧光逆行标记与乙酰胆碱酯酶药理组化显示相结合技术,观察了大白鼠苍白球乙酰胆碱酯酶阳性纤维的起源。向一侧苍白球注入DAPI后,在下列核区内发现胞体既受DAPI标记,同时又含AchE反应阳性产物的细胞(简称荧酶双阳性细胞):斜角带核,丘脑室旁核,丘脑下部室周灰质,中脑腹侧被盖区、黑质、中缝背核和脑桥被盖核。     

猫前脑和脑干向中缝背核的纤维投射

中缝背核在针剌镇痛过程中起重要作用。本文用HRP法,对猫前脑和脑干向中缝背核的纤维投射,作了进一步的研究。 HRP注入中缝背核吻侧部后,在前脑双侧先导回皮质和梨状前区皮质V层出现较多被标记的锥体细胞;缰外侧核出现较密集且形态不一的标记细胞;下丘脑各区(视前区、外侧区、内侧区和后区)也出现散在的标记细胞。 HRP注入中缝背核尾侧部后,除前脑出现标记细胞的部位与HRP注入吻侧部者相同外,在脑干中脑导水管周围灰质、蓝斑,其他中缝核(中央上核,中缝线形核和中缝大核)、臂旁内、外侧核及脑干网状结构等处,也观察到标记细胞。结果表明前脑皮质、缰外侧核、下丘脑各区均有纤维直接投射到中缝背核。中缝背核也接受来自中脑水管周围灰质、蓝斑、其他中缝核等核团的纤维投射;中缝背核吻侧部和尾侧部的传入投射,存在一定的局部定位关系,即中缝背核吻侧部只接受来自前脑的纤维投射,其尾侧部既接受来自前脑的纤维投射,也接受来自脑干的纤维投射。     

大鼠纹状体,中缝核向苍白球和黑质的分叉投射

分别将DAPI和PI注入大鼠同侧苍白球和黑质后,于尾状核、伏隔核、中缝背核和中央上核内见到较多的DAPI和PI单标细胞混杂存在,其中有少量双标细胞     

大白鼠伏隔核乙酰胆碱酯酶阳性纤维的脑干起源

本文报道应用荧光逆行标记和乙酰胆碱酯酶组织化学相结合技术,研究了大白鼠伏隔核乙酰胆碱酯酶阳性纤维的脑干起源。向一侧伏隔核注入荧光示踪剂二盐酸4′,6-双脒基-2-苯吲哚(DAPI)或樱草黄(Pr)。处死前6～8小时肌注二异丙基氟磷酸(DFP)。用含10％福尔马林的磷缓液灌流,连续冠状冰冻切片,Karnovsky-Roots法孵育,荧光显微镜和普通光学显微镜观察同一切片。结果发现,下列核(区)内可见到胞体既受DAPI或Pr逆行标记,同时又呈AChE阳性反应的细胞(简称荧酶双阳性细胞):中脑被盖腹侧区、黑质、中脑尾侧中缝核、脚桥被盖核;脑桥中缝背核、中央上核、被盖网状核、蓝斑;延髓孤束核区、中缝苍白核、延髓网状结构包括旁正中网状核、中央网状核腹侧亚核和外侧网状核。     

外周伤害性刺激后颈髓和三叉神经脊束核尾侧亚核中向中缝背核投射神经元的 c-fos 表达

中缝背核是内源性镇痛系统中的重要核团之一,为了估价该核与外周伤害性信息的传递与调控之间的关系,文内采用荧光金逆行追踪与 FOS 免疫荧光标记相结合的方法进行研究,结果显示将荧光金注入中缝背核后,在三叉神经脊束核尾侧亚核和颈髓后角浅层中可观察到许多荧光金标记神经元的胞体,其中有一部分神经元在给予外周伤害性刺激后被激活而引起 c-fos 表达,该文进一步证明了来自脊髓和三叉神经脊束核尾侧亚核到中缝背核的直接投射至少有一部分与中缝背核的痛觉谓节机制有关。     

外周伤害性刺激后颈髓和三叉神经脊束核尾侧亚核中向中缝背核投 …

中缝背核是内源性镇痛系统中的重要核团之一,为了估计该核与个周伤害性信息的传递与调控之间的关系,文内采用荧光金逆行追踪与ＦＯＳ免疫荧光标记相结合的方法进行研究,结果显示：将荧光金注入中缝背核后,在三叉神经脊束核尾侧亚核和颈髓后角浅层中可观察到许多荧光金标记神经元的胞体,其中有一部分神经元在给予外周伤害性刺激后被激活而引起的ｃ－ｆｏｓ表达,该文进一步证明了来自脊髓和三叉神经脊束核尾侧亚核到中缝背核的直     

大鼠下丘脑向嗅球的传出纤维联系──WGA－HRP和HRP法研究

采用ＷＧＡ－ＨＲＰ和ＨＲＰ逆行追踪法，对２０只ＳＤ大鼠下丘脑向嗅球的投射进行了观察。在同侧下丘脑视前大细胞核均观察到较多的酶标记细胞；同侧下丘脑外侧核和室周核常出现少量酶标记细胞；偶见同侧下丘前核、乳头体外侧核、下丘脑腹内侧核前部、背内侧核腹侧部及弓状核出现少量酶标记细胞。     

大鼠视前内侧区的传入性神经纤维联系,HRP,EB,NY法研究

本文应用轴突逆行运输HRP、EB、NY研究大鼠视前内侧区的传入性神经纤维联系。所用三种示踪剂结果基本一致。结果为:在外侧隔核、外侧嗅束核、杏仁内侧核、下丘脑外侧区、下丘脑腹内侧核和乳头体前腹核内观察到密集的标记细胞。在杏仁皮质核、杏仁中央核、下丘脑室旁核、下丘脑后核、弓状核、乳头体上核、丘脑腹核尾侧部、未定带、腹侧被盖区、脚间核、中缝正中核和背核内观察到较多标记细胞。在中脑中央灰质腹侧部、兰斑核、外侧臂旁核及海马腹下角内观察到少数标记细胞。     

家兔网状脊髓束的起源

本实验用HRP轴突逆行传递法,观察了27只家兔网状脊髓束的起源。实验结果表明,网状脊髓束的起源较为广泛,包括网状结构內侧区、外侧区、中脑网状结构和旁正中网状核,不同核团的标记细胞,数目不等。脊髓不同部位,分别导入HRP时,结果不同,颈體注射例,标记细胞最多的是延體中央腹侧核。腰體注射例,标记细胞最多的是巨细胞网状核。胸髓注射例,网状脑桥尾侧核和脑桥网状嘴侧核中的标记细胞相对增多。在颈髓注射例中,网状结构各核均出现标记细胞。但在腰髓注射例,部分网状结构中的核团无标记细胞。     

大鼠后索核、三叉神经感觉核神经元向小脑和丘脑的分支投射——荧光素双标记法研究

分别把EB和DAPI注入到大鼠的小脑和丘脑,于三叉神经感觉主核、三叉神经脊束核、薄束核、楔内核和楔外核中,见到有较多的EB和DAPI单标神经细胞以及少量的双标细胞。     

大鼠被盖背核的传入性联系——HRP轴突逆行及顺行传递法研究

本研究应用HRP轴突逆行性传递技术,微量注射结合微电泳法,经三种不同入路将酶输入于大鼠的被盖背核,以观察其传入性联系。切片的组织化学处理采用了二氨基苯胺法、联苯胺法、氯化钴二氨基苯胺法和四甲基联苯胺法显色。将HRP输入被盖背核后,在两种输入法和三种入路法切片中均能观察到标记神经元核团的计有:下丘脑外侧核、缰外侧核、束旁核、下丘脑后核、乳头体外侧核、达克谢维奇核、脚间核、中脑导水管周围灰质腹外侧区、中缝背核、舌下神经前置核和孤束核。另外,将HRP分别输入到束旁核和舌下神经前置核后,用HRP轴突顺行传递技术,均可在被盖背核观察到标记终末。从另一角度证实了束旁核—被盖背核和舌下神经前置核—被盖背核间的纤维联系。     

Zincergic innervation from the anterior olfactory nucleus to the olfactory bulb displays plastic responses after mitral cell loss

Zinc ions are selectively accumulated in certain neurons (zinc-enriched neurons). The mouse olfactory bulb is richly innervated by zinc-enriched terminals. Here, the plasticity of the zincergic system was studied in the olfactory bulb of the Purkinje Cell Degeneration mutant mouse, an animal with specific postnatal neurodegeneration of the main projection neurons of the olfactory bulb. The analysis focused particularly on the anterior olfactory nucleus since most centrifugal afferents coming to the olfactory bulb arise from this structure. Zinc-enriched terminals in the olfactory bulb and zinc-enriched somata in the anterior olfactory nucleus were visualized after selenite injections. Immunohistochemistry against the vesicular zinc transporter was also carried out to confirm the distribution pattern of zinc-enriched terminals in the olfactory bulb. The mutant mice showed a clear reorganization of zincergic centrifugal projections from the anterior olfactory nucleus to the olfactory bulb. First, all zincergic contralateral neurons projecting to the olfactory bulb were absent in the mutant mice. Second, a significant increase in the number of stained somata was detected in the ipsilateral anterior olfactory nucleus. Since no noticeable changes were observed in the zinc-enriched terminals in the olfactory bulb, it is conceivable that mitral cell loss could induce a reorganization of zinc-enriched projections coming from the anterior olfactory nucleus, probably directed at balancing the global zincergic centrifugal modulation. These results show that zincergic anterior olfactory nucleus cells projecting to the olfactory bulb undergo plastic changes to adapt to the loss of mitral cells in the olfactory bulb of Purkinje Cell Degeneration mutant mice.     

Zincergic innervation from the anterior olfactory nucleus to the olfactory bulb displays plastic responses after mitral cell loss

Zinc ions are selectively accumulated in certain neurons (zinc-enriched neurons). The mouse olfactory bulb is richly innervated by zinc-enriched terminals. Here, the plasticity of the zincergic system was studied in the olfactory bulb of the Purkinje Cell Degeneration mutant mouse, an animal with specific postnatal neurodegeneration of the main projection neurons of the olfactory bulb. The analysis focused particularly on the anterior olfactory nucleus since most centrifugal afferents coming to the olfactory bulb arise from this structure. Zinc-enriched terminals in the olfactory bulb and zinc-enriched somata in the anterior olfactory nucleus were visualized after selenite injections. Immunohistochemistry against the vesicular zinc transporter was also carried out to confirm the distribution pattern of zinc-enriched terminals in the olfactory bulb. The mutant mice showed a clear reorganization of zincergic centrifugal projections from the anterior olfactory nucleus to the olfactory bulb. First, all zincergic contralateral neurons projecting to the olfactory bulb were absent in the mutant mice. Second, a significant increase in the number of stained somata was detected in the ipsilateral anterior olfactory nucleus. Since no noticeable changes were observed in the zinc-enriched terminals in the olfactory bulb, it is conceivable that mitral cell loss could induce a reorganization of zinc-enriched projections coming from the anterior olfactory nucleus, probably directed at balancing the global zincergic centrifugal modulation. These results show that zincergic anterior olfactory nucleus cells projecting to the olfactory bulb undergo plastic changes to adapt to the loss of mitral cells in the olfactory bulb of Purkinje Cell Degeneration mutant mice.