Transmitter Release Associated with Long-term Synaptic Depression in Rat Corticostriatal Slices

Using a corticostriatal slice preparation, we have recently shown that tetanic stimulation of the corticostriatal pathway produces long-term depression (LTD) of striatal excitatory synaptic transmission. In the present study we have analysed the relationship between LTD and the striatal release of different endogenous transmitters. Samples of perfusate were collected via a small cannula placed just above the surface of the striatal slice close to the recording electrode, and were analysed by HPLC. The high-frequency stimulation (100 Hz, three trains, 3 s duration, 20 s intervals) used to induce LTD caused a significant but transient increase in the release of both excitatory (aspartate and glutamate) and inhibitory (glycine and GABA) amino acid transmitters. Tetanic stimulation also produced a significant, but transient increase in the release of endogenous dopamine. We conclude that the tetanic stimulation of the corticostriatal pathway is able to induce a large but transient release of excitatory amino acids and of dopamine, whose participation in the induction of striatal LTD has been demonstrated previously. Moreover, the maintenance of this form of synaptic plasticity does not seem to require a sustained change in transmitter release.     

Excitatory amino acid receptor regulation after subthalamic nucleus lesions in the rat

The subthalamic nucleus plays a pivotal role in the regulation of basal ganglia output. Recent electrophysiologic, lesion and immunocytochemical studies suggest that the subthalamic nucleus uses an excitatory amino acid as a neurotransmitter. After complete ablation of the subthalamic nucleus, we have examined the NMDA, AMPA, kainate and metabotropic subtypes of excitatory amino acid receptors in two major subthalamic projection areas (globus pallidus and substantia nigra pars reticulata) with quantitative autoradiography. Two weeks after ablation, binding sites for [³H]AMPA and [³H]kainate increased in substantia nigra pars reticulata ipsilateral to the lesion. In globus pallidus on the lesioned side, [³H]glutamate binding to the NMDA recognition site decreased. The results suggest that glutamate receptors regulate after interruption of subthalamic nucleus output.     

Brain MR imaging in patients with hepatic cirrhosis: relationship between high intensity signal in basal ganglia on T1-weighted images and elemental concentrations in brain

In patients with hepatic cirrhosis, the globus pallidus and putamen show high intensity on T1-weighted MRI. While the causes of this high signal have been thought to include paramagnetic substances, especially manganese, no evidence for this has been presented. Autopsy in four cases of hepatic cirrhosis permitted measurement of metal concentrations in brain and histopathological examination. In three cases the globus pallidus showed high intensity on T1-weighted images. Mean manganese concentrations in globus pallidus, putamen and frontal white matter were 3.03 ± 0.38, 2.12 ± 0.37, and 1.38 ± 0.24 (μg/g wet weight), respectively, being approximately four- to almost ten-fold the normal values. Copper concentrations in globus pallidus and putamen were also high, 50 % more than normal. Calcium, iron, zinc and magnesium concentrations were all normal. The fourth case showed no abnormal intensity in the basal ganglia and brain metal concentrations were all normal. Histopathologically, cases with showing high signal remarkable atrophy, necrosis, and deciduation of nerve cells and proliferation of glial cells and microglia in globus pallidus. These findings were similar to those in chronic manganese poisoning. On T1-weighted images, copper deposition shows no abnormal intensity. It is therefore inferred that deposition of highly concentrations of manganese may caused high signal on T1-weighted images and nerve cell death in the globus pallidus. Received: 12 August 1996 Accepted: 17 December 1996     

交感神经节培养的形态学观察

目的：观察交感神经节在体外培养中的生长和形态学特点。方法：无菌，取新生大鼠椎旁交感神经节，用Ｍａｘｉｍｏｗ培养法在相差显微镜下动态观察７天。终止２后，用Ｈｏｌｍｅｓ还原银染色法显示神经纤维。结果：交感神经节在壁后１２－１８ｈ开始生长，２４－４８ｈ由交感神经节长出的纤维长约０．５ｍｍ，７２－９６ｈ可见神经纤维伸长到１－２ｍｍ以上，并呈放射状向四周延伸。Ｈｏｌｍｅｓ还原银染色的标本中可见大量银染的神经     

Is progression in postencephalitic parkinson's disease late and age-related?

Summary Follow-up data are presented of ten patients with autopsy-proven postencephalitic Parkinson's syndrome (PEP) (mean age at death: 56.0 years) with regard to motor and psychic deterioration over a period of institutional observation between 3 and 30 years. Four patients showed deterioration of their Hoehn-Yahr score of at least one grade. These patients did not differ statistically with respect to age of occurrence of lethargic encephalitis, interval to PEP, age at start of PEP, duration of survival with PEP, and age at death. Motor deterioration in these patients seems to be attributed more to inherent disease progression, rather than to an age-related process. Clinical and pathological evidence for this conclusion is presented.     

大鼠神经系统发育过程中神经元特异性烯醇酶的出现和意义

用自行提纯的人脑和牛脑神经元特异性烯醇酶(NSE)分别免疫家兔,制备兔抗人和抗牛NSE血清(抗NSEh和抗NSEb)。以PAP免疫组织化学染色,系统观察3O只发育出SD大鼠的脑、脊髓与脊神经节。发现NSE最先出现于胚胎15d的脊神经节神经元,随后相继出现于三叉神经节、脊髓、嗅皮质、海马、扣带回和外侧皮质神经元。表明NSE先后出现于周围神经和中枢神经系统,由脊髓向大脑、原始皮质及新皮质发展的顺序,与神经系统发育过程中的头向发展规律相一致。     

Orthofix-微型外固定器治疗Bennett骨折31例

目的分析应用Orthofix-微型器治疗第一掌骨基底部Bennett骨折的临床疗效。方法收集2009年1月~2013年1月我院31例采用Orthofix-微型器治疗的第一掌骨基底部Bennett骨折患者。记录患者年龄、性别等基线资料,以及术后上肢臂、肩、手功能调查量表(Disabilities of the arm,shoulder and hand,DASH)评分,随访终末期采用指总关节活动度(Total action movement,TAM)评分。结果随访6~24个月,平均14.4月,手术时间为18~40分钟,平均29.1分钟,术中出血量10~30m L,平均14.5m L。术后3月、术后6月及终末期DASH评分之间比较,差异均有统计学意义(0.05)。随访终末期,其中26例解剖复位,5例骨折对线良好,TAM评分优22例,良7例,差2例。随访期间未发生桡神经浅支损伤、钉道感染等并发症。结论 Orthofix-微型外固定器治疗Bennett骨折操作简单、疗效满意。     

Immunoreactive somatostatin-28(1-12) is increased in Huntington's disease

Somatostatin-28(1-12) concentrations were measured in Huntington's disease (HD) postmortem tissue using a specific radioimmunoassay. Concentrations of immunoreactive somatostatin-28(1-12) were significantly increased in the caudate and putamen but were unchanged in cortical areas A9 and A17. Since somatostatin-28(1-12) terminates with the amino acids Arg-Glu-OH, we examined whether this dodecapeptide compound might exert a neurotoxic effect. Injections of somatostatin-28(1-12) into rat striatum showed no evidence of histologic damage.