损毁成体鸽下丘脑腹内侧核对神经元增生的影响

本实验应用（＾３Ｈ）放射自显影和免疫组织化学方法首次报道了高等脊椎动物成体鸟脑损伤引起神经元增生的观察结果。电损毁非鸣禽成体环鸽下丘脑腹内侧核后能引起端脑外侧室带区中（＾３Ｈ）标记细胞的大量增生和在端脑尾部ＬＶＺ中的特异性分布。     

黄雀端脑听区神经联系的研究

本文用ＨＲＰ顺、逆行追踪法研究鸣禽黄雀（Ｇａｒｄｕｅｌｉｓ ｓｐｉｎｕｓ）端脑听区（Ｆｉｅｌｄ ‘Ｌ’，Ｌ）的神经联系。将ＨＲＰ微电泳入Ｌ区，在同侧丘脑卵圆核（Ｎｕｃｌｅｕｓ ｏｖｏｉｄａｌｉｓ，ｐａｒｓ ｃｅｎｔｒａｌｉｓ，ＯＶ）等处见到逆行标记细胞；在端脑上纹状体腹侧尾部（Ｈｙｐｅｒｓｔｒｉａｔｕｍ ｖｅｎｔｒａｌｅ ，ｐａｒｓ ｃａｕｄａｌｅ，ＨＶｃ）等处见到顺行标记终末。结果表明，端脑Ｌ区     

鸽丘脑听觉中继核团传出神经投射的研究

应用神经示踪物生物素标记的葡聚糖对环鸽丘脑听觉中继核团的传出神经投射进行了研究。结果发现：（１）丘脑卵圆核的传出纤维投射至端脑新纹状体内侧的Ｌ２听区;（２）卵圆核壳的传出纤维投射至Ｌ１、Ｌ３和部分Ｌ２听区,在Ｌ区周围亦存在许多标记终末;（３）尾侧卵圆核壳的传出投射参与了卵圆核壳的形成并发出二束纤维分别投射至下丘脑腹内侧核和端脑新纹状体Ｌ区外侧的旁听区。本实验结果首次揭示在鸟类丘脑听中继核团、端脑新     

黄雀中脑及丘脑听性核团的纤维联系

本文用ＨＲＰ顺、逆行追踪方法，研究黄雀中脑下丘中央核（ＩＣｃ）及丘脑卵圆核（ＯＶ）的传入联系及ＯＶ向端脑的投射。将ＨＲＰ微电泳入ＩＣｃ，在延髓角状核、层状核及脑桥外侧丘系核复合体出现了密布的标记细胞，在ＯＶ及卵圆核的腹内侧部见到密集的标记终末，在对侧ＩＣｃ有许多的标记细胞及终末。将ＨＲＰ微电泳入ＯＶ，除在ＩＣｃ有大量的标记细胞外，在端脑Ｌ听区等处见到密集的标记终末。结果表明，ＩＣｃ接受角状核、层状核和外侧丘系核复合体的传入投射，由它发出的纤维投射到ＯＶ及卵圆核的腹内侧部，双侧ＩＣｃ间有往返联系，从ＯＶ发出的纤维投射至端脑的Ｌ听区。Ｌ听区可能是听觉的高位中枢。     

γ-氨基丁酸对离体大鼠延髓头端腹外侧区神经元单位放电的抑制作用

在７３张脑片上观察了γ－氨基丁酸（ＧＡＢＡ）对１０６个延髓头端腹外侧区（ＲＶＬＭ）神经元单位放电的影响。外源性的ＧＡＢＡ（０．１￣３．０ｍｍｏｌ／Ｌ）抑制了１０６神经元中的８４个神经元的电活动,这些抑制效应呈剂量－反应关系。ＧＡＢＡ的抑制效应大部分可被ＧＡＢＡＡ受体选择性拮抗剂荷苞牡丹碱甲基碘化物（ＢＭＩ）和Ｃｌ＾－通道阻断剂印防己毒素（ＰＴＸ）所阻断,而单独灌流ＢＭＩ和ＰＴＸ对ＲＶＬＭ神经元主要     

P物质在谷氨酸兴奋外侧下丘脑—穹窿周围区引起的升压反…

Ｐ物质（ＳＰ）能神经元及其轴突末和受体广泛分布于很多心血管中枢。外侧下丘脑含ＳＰ能神经元,外侧下丘脑投射的升压区内又存在ＳＰ能纤维及ＳＰ受体;因此本工作检验ＳＰ在外侧下丘脑升压反应中的作用。实验显示：（１）Ｌ－谷氨酸兴奋外侧下天脑的穹窿周围区（ＬＨ／ＰＦ）或将ＳＰ分别注入各ＬＨ投射区,蓝斑（ＬＣ）、臂旁核（ＮＰＢ）或 导不管周围灰质（ＰＡＧ）均引起升压反应;（２）「Ｄ－Ｐｒｏ＾２,Ｄ－Ｐｈｅ＾７,     

一氧化氮抑制内皮素促血管平滑肌细胞增殖作用的信号转导途径

培养的家兔胸主动脉血管平滑肌细胞（ＶＳＭＣ）分别以内皮素（ＥＴ－１）、一氧化氮（ＮＯ）前体Ｌ－Ａｒｇ和ＮＯ供体ＳＩＮ－１刺激,或用ＥＴ－１＋Ｌ－Ａｒｇ、ＥＴ－１＋ＳＩＮ－１联合刺激,测ＶＳＭＣ＾３Ｈ－ＴｄＲ掺入、丝裂素活化蛋白激酶（ＭＡＰＫ）活性及蛋白激酶Ｃ（ＰＫＣ）活性的改变,以研究ＮＯ抑制ＥＴ－１促ＶＳＭＣ增殖作用的信号转导途径。结果表明：（１）ＥＴ－１ １０＾－８ｍｏｌ／Ｌ单独刺激,＾３Ｈ－     

鼠源抗HFRSV衣壳蛋白McAbF3株单链抗体基因克隆构建及表达

为了获得原抗ＨＦＲＳＶ衣壳蛋白ＭｃＡｂＦ３＾１株轻链可变区基因,由连接肽体外连接获得单链抗体基因,在大肠杆菌中表达,从鼠源抗ＨＦＲＳＶ衣壳蛋白ＭｃＡｂＦ３株细胞中分离总ＲＮＡ,以ｏｌｉｇｏ（ｄＴ）１８为引物逆转录成ｃＤＮＡ,通过ＰＣＲ扩增出抗体的轻链（ＶＬ）和重链可变区（Ｖ１１）基因,由连接本外连接获得单链抗体（ＳｅＦｖ）基因。将此单链抗体（ＳｅＦｖ）基因插入原核表达载体ＰＥＴ２８ａ,经大肠杆菌（     

腺苷对缺氧时海马神经元内游离Ca^2＋的影响

实验用Ｆｌｕｏ－３负载细胞,在激光扫描共聚焦显微镜下直接监测缺氧后分散培养的大鼠海马ＣＡ１区神经元内游离Ｃａ＾２＋浓度（［Ｃａ＾２＋］ｉ）的变化,观察腺苷对这种变化的影响并初步探讨其作用机制。结果发现,急性缺氧使海马神经元［Ｃａ＾２＋］ｉ显著升高;腺苷（１００μｍｏｌ／Ｌ）明显抑制缺氧引起的［Ｃａ＾２＋］ｉ增高,腺苷Ａ１受体拮抗剂ＣＰＴ以及Ｋ＾＋通道阻断剂４－ＡＰ和ＡＴＰ敏感性Ｋ＾＋通道阻断剂ｇｌ     

光氧化胁迫下几种植物叶片的超氧自由基产生速率和光合特性

以甲基藉精（ＭＶ）Ｏ－１ｍｍｏｌ／Ｌ在１５００μｍｏｌ ｍ＾－２ａ＾－１光下处理Ｃ３植物花生、水稻和Ｃ４植物玉米、甘蔗的叶圆片３０ｍｍ,Ｏ２＾２＋产生速率随ＭＶ浓度提高而加快ＭＶ浓度超过１０μｍｏｌ／Ｌ,光合放氧出现负植并持续增大。光氧化作用降低叶绿素荧光参数ＦＶ／Ｆｍ,ΦＰＳⅡ和ｑｐ,而ｑＮ则或提高（Ｃ３植物,ＭＶ１０μｍｏｌ／Ｌ）或几平下）。热耗散系数ＫＤ的变化与ＱＮ相似。秘Ｃ４植物相比,Ｃ３     

Proliferation "hot spots" in adult avian ventricular zone reveal radial cell division

Neurogenesis in the adult avian brain is restricted to the telencephalon. New neurons originate in the ventricular zone (VZ) from cells that have not been identified. We mapped the position of [3H]thymidine-labeled cells in the walls of the ventricles of the adult canary brain. Labeled VZ cells were restricted to the telencephalon (lateral ventricles) and concentrated in "hot spots". The coincidence of these hot spots with regions rich in radial cells suggested that radial cells may be the cells undergoing mitosis. We used smears prepared from fragments of the VZ containing the hot spots to show directly that radial cells accumulate [3H]thymidine. In addition, grain counts at different survival times demonstrated that these cells divide. Hot spots of VZ cell division also coincided with sites of neuronal origin. We suggest that radial cell division may give rise to new neurons.     

雌百灵端脑新生神经前体细胞的产生和分布并与白腰文鸟的比较

用BrdU标记DNA的ABC免疫细胞化学方法,观察雌性蒙古百灵端脑神经前体细胞的产生和分布特点,并与白腰文鸟作比较。结果如下:1.在百灵和白腰文鸟胸肌注射BrdU短时程组(存活1天),在端脑室带区外侧壁(LVZ)有大量的标记细胞,新生神经细胞起源于端脑室带区(VZ)中的增殖细胞层,并在纹状体腹侧的VZ形成标记细胞增殖热点,如在百灵和白腰文鸟靠近中缝线处的外侧纹状体(LSt)与内侧纹状体(MSt)腹侧的LVZ形成标记最多的‘第1增殖热点’区;在靠近中缝线处LVZ的头端形成密集的新生标记细胞,形成‘第2增殖热点’区;在百灵LSt尾端的LVZ标记细胞形成‘第3增殖热点’,但白腰文鸟此脑区的标记细胞较少。2.在百灵胸肌注射BrdU长时程组中5天起,大量的LVZ的标记细胞开始迁移,存活5-30天期间在高级发声中枢(HVc)和高位发声运动中枢-古纹状体栎核(RA)有新生标记细胞,在端脑靠近LVZ的区域有较多的标记细胞。但在雌性白腰文鸟胸肌注射BrdU存活30天期间,在HVC、RA内未见到标记细胞。结果提示雌百灵端脑HVc和RA不断地产生新生神经细胞,这可能与雌性需要不断地感知、识别雄百灵鸣唱的新语句有关,而白腰文鸟不需要这种功能。     

Expression of PTTG and prc1 genes during telencephalic neurogenesis

We present the first time/space analysis using in situ hybridization for PTTG and prc1 genes during development of the mouse telencephalon. During the stages E11.5-E13.5 PTTG and prc1 are expressed in most tissues of the embryo. Within the telencephalon, PTTG and prc1 are found exclusively inside of the ventricular zone (VZ). The intensity of the expression of both genes in the ventricular zone reaches its peak by E15.5. Expression starts to decrease by E18.5, it is still visible at least up to P2 and not detectable in the adult brains. Expression of the prc1 gene, but not that of the PTTG, is also found in the mitoticaly active cells outside of the VZ within the telencephalon. Most of the cells expressing the PTTG gene were found in the lower part of the ventricular zone suggesting that the level of PTTG mRNA is regulated during different phases of the mitotic cycle.     

The impact of deafness to the survival of the newborn cells in the brain of juvenile white-rumped munia, Lonchura striata

In white-rumped munia, early auditory experience is critical for normal song development. New neurons are constantly added to the telencephalon in juveniles. We examined the potential role of auditory experience in regulating the developmental changes in the song nuclei and the survival of newborn cells. We chose two special days, postnatal day 23 and 37, at which we deafened the birds through bilateral cochlea removal. All birds were injected with the cell birth marker BrdU two weeks before the lesion surgeries, and then were killed two weeks or one month later. The BrdU-positive cells were distributed throughout the brain, including the high vocal center (HVC), Lobus parolfactorius and the ventricle zone (VZ) in telencephalon, the granular cell layer (GCL) of cerebellum. Moreover, these BrdU-positive cells in the GCL could self-renew. However, the nucleus robustus archistriatalis (RA) did not sprout new neurons in juvenile. In telencephalon except the VZ, 41 percent of BrdU-positive cells were NeuN-positive, too. Deafness had no significant effect on development of HVC and RA, the distribution of new cells, and the survival of new cells in telencephalon. From these data, we propose that auditory deprivation could not affect the survival of new cells of telencephalon within one month. Surprisingly, we found deafness had a complex and dramatic effect on the number of new cells in cerebellum. Deafness at postnatal day 23 could increase the number of new cells in the GCL, while deafness at postnatal day 37 decreased the number.     

Effects of excess thyroid hormone on cell death,cell proliferation,and new neuron incorporation in the adult zebra finch telencephalon

Widespread telencephalic neuronal replacement occurs throughout life in birds. We explored the potential relationship between thyroxine (T4) and cell turnover in the adult male zebra finch. We found that many cells in the zebra finch brain, including long-projection neurons in the high vocal center (HVC), stained positively with an antibody to thyroid hormone receptors (TR). Labeling was generally weak in the ventricular zone (VZ) that gives rise to new neurons but some proliferative VZ cells and/or their progeny, identified by [3H]-thymidine labeling, co-labeled with anti-TR antibody. Acute T4 treatment dramatically increased the number of pyknotic and TUNEL-positive cells in HVC and other telencephalic regions. In contrast, degenerating cells were never observed in the archistriatum or sub-telencephalic regions, suggesting that excess T4 augments cell death selectively in regions that show naturally occurring neuronal turnover. VZ mitotic activity was not altered shortly after acute T4 treatment at a dosage that stimulated cell death, although [3H]-labeling intensity per cell was slightly reduced. Moreover, the incorporation rates for neurons formed shortly before or after acute hormone treatment were no different from control values. Chronic T4 treatment resulted in a reduction in the total number of HVC neurons. Thus, hyperthyroidism augmented neuronal death, which was not compensated for by neuronal replacement. Collectively, these results indicate that excess T4 affects adult neuronal turnover in birds, and raises the possibility that thyroxine plays an important role in the postnatal development of the avian brain and vocal behavior.     

The studies on neurogenesis induced by brain injury in adult ring dove

INTRODUCTIONItisacommonstatementthatillhighervertebratestheCNScompletesneuronaldevelopmentduringthepre--andprenatalperiods.Preliminaryworkshowedthatneurogenesisconfinuedinthebrainofsongbirdduringadulthood.Manynewbornneuronsareincorporatedintothevocal-cont…     

Tangential migration and proliferation of intermediate progenitors of GABAergic neurons in the mouse telencephalon

In the embryonic neocortex, neuronal precursors are generated in the ventricular zone (VZ) and accumulate in the cortical plate. Recently, the subventricular zone (SVZ) of the embryonic neocortex was recognized as an additional neurogenic site for both principal excitatory neurons and GABAergic inhibitory neurons. To gain insight into the neurogenesis of GABAergic neurons in the SVZ, we investigated the characteristics of intermediate progenitors of GABAergic neurons (IPGNs) in mouse neocortex by immunohistochemistry, immunocytochemistry, single-cell RT-PCR and single-cell array analysis. IPGNs were identified by their expression of some neuronal and cell cycle markers. Moreover, we investigated the origins of the neocortical IPGNs by Cre-loxP fate mapping in transgenic mice and the transduction of part of the telencephalic VZ by Cre-reporter plasmids, and found them in the medial and lateral ganglionic eminence. Therefore, they must migrate tangentially within the telencephalon to reach the neocortex. Cell-lineage analysis by simple-retrovirus transduction revealed that the neocortical IPGNs self-renew and give rise to a small number of neocortical GABAergic neurons and to a large number of granule and periglomerular cells in the olfactory bulb. IPGNs are maintained in the neocortex and may act as progenitors for adult neurogenesis.     

Effects of excess thyroid hormone on cell death,cell proliferation,and new neuron incorporation in the adult zebra finch telencephalon

Widespread telencephalic neuronal replacement occurs throughout life in birds. We explored the potential relationship between thyroxine (T₄) and cell turnover in the adult male zebra finch. We found that many cells in the zebra finch brain, including long‐projection neurons in the high vocal center (HVC), stained positively with an antibody to thyroid hormone receptors (TR). Labeling was generally weak in the ventricular zone (VZ) that gives rise to new neurons but some proliferative VZ cells and/or their progeny, identified by [³H]‐thymidine labeling, co‐labeled with anti‐TR antibody. Acute T₄ treatment dramatically increased the number of pyknotic and TUNEL‐positive cells in HVC and other telencephalic regions. In contrast, degenerating cells were never observed in the archistriatum or sub‐telencephalic regions, suggesting that excess T₄ augments cell death selectively in regions that show naturally occurring neuronal turnover. VZ mitotic activity was not altered shortly after acute T₄ treatment at a dosage that stimulated cell death, although [³H]‐labeling intensity per cell was slightly reduced. Moreover, the incorporation rates for neurons formed shortly before or after acute hormone treatment were no different from control values. Chronic T₄ treatment resulted in a reduction in the total number of HVC neurons. Thus, hyperthyroidism augmented neuronal death, which was not compensated for by neuronal replacement. Collectively, these results indicate that excess T₄ affects adult neuronal turnover in birds, and raises the possibility that thyroxine plays an important role in the postnatal development of the avian brain and vocal behavior. © 2002 Wiley Periodicals, Inc. J Neurobiol 51: 323–341, 2002