Synaptic reorganization in the medial amygdaloid nucleus after lesion of the accessory olfactory bulb of adult rat. II. New synapse formation in the medial amygdaloid nucleus by fibers from the bed nucleus of the stria terminalis

The rearrangement of terminations from the bed nucleus of stria terminalis (BST) was examined in the medial amygdaloid nucleus (MAN) at 2 months following the lesion of the accessory olfactory bulb (AOB) using an electron microscopy and degeneration study. At 2 days following a BST lesion, the number of degenerating synapses was 0.7 ± 0.1 (mean±S.E.M.) per unit area (2500 μm² in the molecular layer, and 3/0 ± 0.3 in the cellular part. At 2 months after an AOB lesion, the degenerating synapses from the AOB had completely disappeared from the MAN. The BST was then lesioned at 2 months after the AOB lesion and, 2 days following this BST lesion, the degenerating synapses were counted in MAN. The numbers observed were 3.3 ± 0.6 per unit area in the molecular layer and 4.5 ± 0.4 in the cellular part. Therefore, the number of these degenerating synapses increased significantly within the molecular layer, though, in the cellular part the number of synapses was not significantly elevated over control. No differences in postsynaptic profiles (ratio of synapses on dendritic spine to dendritic shaft) were observed after the AOB lesion. These results indicate that the BST fibers formed new synapses in the molecular layer following the denervation of AOB fibers. The possibility of new synapse formation by other afferent fibers in addition to the AOB fibers is discussed as is the relationship between lesion induced synaptic reorganization and functional recovery after injury.     

Capillary hemangioblastoma: histogenesis of stromal cells

Summary The histogenesis of stromal cells in capillary hemangioblastoma has been the subject of debate. The light and electron microscopic studies of hemangioblastomas presented here showed pericytic and leiomyoblastic features in stromal cells. Cells cultured by the monolayer method showed similar features to those of the original tumors. Immunohistochemical studies for glial fibrillary acidic protein and factor VIII/von Willebrand factor indicated that stromal cells were antigenically distinct from astrocytes and endothelial cells. These findings suggest that stromal cells are closely related to pericytes and smooth muscle cells, and support Rhodin's speculation that pericytes serve as a precursor to smooth muscle cells.     

The cholinergic innervation of the rat fascia dentata: identification of target structures on granule cells by combining choline acetyltransferase immunocytochemistry and Golgi impregnation

A monoclonal antibody against choline acetyltransferase (ChAT), the acetylcholine-synthesizing enzyme, was used to study cholinergic synapses on identified (Golgi stained) granule cells in the rat fascia dentata. Choline acetyltransferase immunocytochemistry was applied to 40-microns Vibratome sections cut perpendicular to the longitudinal axis of the hippocampus. Light microscopy revealed fine varicose ChAT-immunoreactive axons in all layers of the fascia dentata, i.e., in the stratum moleculare, the stratum granulosum, and the subgranular polymorph zone. Most fibers were observed in the vicinity of granule cell bodies where they ran mainly parallel to the granular layer. Next, the immunostained Vibratome sections were sandwiched between small pieces of Parafilm and piled to form a block that was covered with agar and Golgi stained. After that, the sections were separated by cutting away the agar and removing the Parafilm. Sections containing well-impregnated granule cells were gold-toned (Fairén et al., '77), embedded in Araldite, and subjected to ultrathin sectioning for electron microscopy. A total of 14 gold-toned granule cells were examined in the electron microscope for synaptic contacts with cholinergic afferents. Choline acetyltransferase-immunoreactive axon terminals were observed that established symmetric synaptic contacts with the cell bodies and dendritic shafts of the gold-toned identified granule cells. Two types of contact were observed on spines arising from gold-toned granule cell dendrites. Immunoreactive terminals established asymmetric synaptic contacts with the head of small spines and symmetric contacts with the stalk of large, complex spines. The boutons forming asymmetric synaptic contacts with the cup-shaped spine head of the complex spines were not found to be immunoreactive. Our results demonstrate that cholinergic fibers to the rat fascia dentata establish characteristic types of synaptic contact with different postsynaptic elements of granule cells, suggesting a complex function of this afferent system.     

快速眼动睡眠剥夺后大鼠脑内神经元骨架蛋白及超微结构的变化

目的探讨经历不同时间快速眼动（REM）睡眠剥夺对大鼠皮质及海马各区神经元形态结构的影响。方法选择微管相关蛋白（MAP2）和神经丝（NF）作为正常神经元结构的标识物，利用免疫组织化学法和Western blot技术观察REM睡眠剥夺1、3、5、7 d4个时间点大鼠皮质及海马MAP2和NF表达的时空变化规律。同时运用电镜技术观察睡眠剥夺后神经元超微结构的变化。我们的实验是用改良的多平台睡眠剥夺模型进行REM睡眠剥夺，结合免疫组织化学染色技术和蛋白质电泳以及电镜超微结构分析。结果REM睡眠剥夺后5d大鼠皮质、海马CA1及齿状回神经元结构蛋白MAP2和NF表达较对照组明显减少（P〈0．05）；电镜神经元核仁偏位，胞质中出现少量肿胀的线粒体和内质网；部分神经轴突的髓鞘溶解与浓集。环境对照组、REM睡眠剥夺5d和7d组，皮质中超微结构改变的神经元所占比例分别为1．2％、3．6％和5．8％。结论REM睡眠剥夺能够导致大鼠脑内神经元的超微结构发生异常变化。     

Extremely Well Differentiated Papillary Adenocarcinoma of the Lung with Prominent Cilia Formation

We describe a 54-year-old woman with primary pulmonary adenocarcinoma showing a characteristic papillary architecture and prominent cilia formation. Immunohistochemically, the tumor cells were positive for carcinoembryonic antigen (CEA), epithelial membrane antigen (EMA) and Leu Ml, and negative for lactoferrin and surfactant apoprotein. An ultrastructural study also indicated differentiation toward bronchial surface epithelial cells. To our knowledge, this type of neoplasm has not been reported as peripheral-type adenocarcinoma of the lung. Acta Pathol Jpn 42: 745–750, 1992.     

二乙基二硫代氨基甲酸钠对沙土鼠脑缺血再灌注损伤的影响

沙土鼠脑缺血60min后,脑组织氧自由基和MDA含量无明显升高,而Mn-SOD的活性下降。缺血60min再灌注5min时,氧自由基显著升高。再灌注30min时,MDA的生成显著增多,Mn-SOD和Cu,Zn-SOD活性显著降低。缺血前15 min,iv DTC对缺血再灌注脑组织中氧自由基和MDA升高有显著抑制作用,对Mn-SOD活性有显著保护作用,且呈剂量依赖关系。     

The Glutamatergic Innervation of Oxytocin- and Vasopressin-secreting Neurons in the Rat Supraoptic Nucleus and its Contribution to Lactation-induced Synaptic Plasticity

The present ultrastructural study analysed the distribution of glutamatergic synapses on oxytocin- and vasopressin-secreting neurons in the rat supraoptic nucleus (SON) after post-embedding immunogold labelling for glutamate and GABA, oxytocin or vasopressin. About 20% of SON axo—somatic synapses were enriched in glutamate immunoreactivity, visible over synaptic-like vesicles, mitochondria and synaptic densities. Double labelling for glutamate and GABA showed that putative glutamatergic terminals were distinct from GABAergic terminals. In ultrathin sections stained for glutamate and either oxytocin or vasopressin, the proportion of glutamatergic synapses was similar on oxytocinergic and vasopressinergic somata in virgin rats under basal conditions of peptide release as well as in lactating rats, in which oxytocin secretion is enhanced. Cross-sectional soma areas were significantly increased in lactating rats: oxytocinergic profiles were, on average, ˜40% larger than in virgin rats. However, the incidence of axo—somatic glutamatergic synapses (assessed as mean number of synapses per 100 μm of plasmalemma or proportion of somatic surface apposed to synaptic active zones) did not diminish, indicating that there was a compensatory increase of synapses during lactation. Also, we found an increase in the number of glutamatergic terminals making synaptic contact simultaneously onto two or more oxytocinergic elements in the same plane of section. Our observations therefore indicate that SON oxytocinergic and vasopressinergic neurons are innervated to a similar extent by a relatively large proportion of glutamatergic synapses. They reveal, moreover, that glutamatergic afferents participate in the lactation-induced synaptic plasticity of the oxytocinergic system.     

Morphological study of neocortical areas in Rett syndrome

Various neocortical areas from four females aged 16–24 years with Rett syndrome (RS) were investigated and compared with brains of therapy-resistant partial epilepsy (TRPE) patients (18–25 years), infantile autism (IA), and control brains (24 and 58 years). The cytoarchitecture of area 10 (frontal), area 21 (temporal), area 4 (primary motor cortex), and area 17 (primary visual cortex) was studied by the combined Klüver-Barrera (luxol fast blue and cresyl violet) standard procedure. Autofluorescence of lipofuscin, immunofluorescence of synaptic vesicle proteins [synaptophysin (p38)] and lectin-stained (Wisteria floribunda agglutinin) perineuronal nets (PNs) were studied in the cortices using dual-channel confocal laser scanning microscopy. The brains of RS females show various types of morphological/cytoarchitectonical abnormalities of single pyramidal neurons in layers II–III, and V–VII of different cortical areas. The abnormalities include mild losses of pyramidal neurons, more pronounced in layers II and III than in layers V and VII, and more evident in frontal and temporal areas than in the visual cortex. Microdysgenesis, including abnormalities due to neuronal migration disorders, was not found in RS, in contrast to the observations in TRPE patients, strongly indicating that RS is not a neuronal migration disorder. Lipofuscin distribution was normal but amounts were lower in RS cases than in control and TRPE brains. PNs were less expressed in cortices of the IA case, but were clearly overexpressed in the motor cortex of RS. Quantitative analysis of p38 showed a decrease in the area occupied by p38 immunoreactivity by 20–40% in RS compared with controls. It is concluded that RS could best be explained by a postnatal synaptogenic developmental deficiency; the basic defect, however, is still completely unknown. Received: 26 February 1996 / Revised, accepted: 11 July 1996     

Sural nerve biopsies in Guillain-Barre syndrome: axonal degeneration and macrophage-associated demyelination and absence of cytomegalovirus genome.

T-cell infiltration was detected by immunohistochemistry in only 2 of 10 sural nerve biopsies from patients with Guillain-Barré syndrome (GBS). The number of endoneurial macrophages, identified by the monoclonal antibody MAC 387, was increased, compared with the number in 10 cases of axonal neuropathy. Macrophage-associated demyelination was identified in 7 and axonal degeneration in 8 cases. Cytomegalovirus (CMV) genome was not detected with the polymerase chain reaction.