Molecular and chemical neuropathology最新文献_第10页

Ultrastructural localization of butyrylcholinesterase in senile plaques in the brains of aged and Alzheimer disease patients. 老年和阿尔茨海默病患者大脑老年斑中丁基胆碱酯酶的超微结构定位。

Molecular and chemical neuropathology Pub Date : 1997-04-01 DOI: 10.1007/BF02815095

P Gómez-Ramos, M A Morán

引用次数: 42

Spinal cord myelin is vulnerable to decompression. 脊髓髓磷脂容易受到减压的影响。

Molecular and chemical neuropathology Pub Date : 1997-04-01 DOI: 10.1007/BF02815103

J P Bond, D A Kirschner

{"title":"Spinal cord myelin is vulnerable to decompression.","authors":"J P Bond, D A Kirschner","doi":"10.1007/BF02815103","DOIUrl":"https://doi.org/10.1007/BF02815103","url":null,"abstract":"Spinal cord white matter is the major site of tissue damage resulting from decompression sickness (DCS or \"the bends\"). Damage is thought to result from bubble nucleation within the tissue. Why DCS occurs predominantly in the spinal cord and not in the brain is not known; neither is the exact pathological mechanism by which the spinal cord is damaged, nor how multiple sclerosis (MS)-like symptoms may ensue. To investigate the molecular basis of white matter damage, we subjected myelinated mouse tissues to varying durations of decompression, and then after recompression to one atmosphere, examined them for changes in myelin structure and composition. X-ray diffraction showed that the myelin period in spinal cord decreased by 4%, whereas those of optic and sciatic nerves were stable. The change in period was accompanied by a change in membrane bilayer profile--i.e., relative to control, the width of the bilayer decreased by approximately 6 A, whereas the interbilayer spaces each increased by approximately 3 A. The changes in electron density levels suggested a redistribution of matter from the interbilayer spaces into the lipid headgroup layers. By contrast with these structural changes, sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and high-performance thin layer chromatography (HPTLC) revealed no noticeable change in myelin composition--i.e., there was no release of myelin-specific proteins or lipids. Our findings indicate that spinal cord myelin has an inherent structural vulnerability that may facilitate the targeting of this tissue during pressure changes.","PeriodicalId":18736,"journal":{"name":"Molecular and chemical neuropathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02815103","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20112428","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

The effects of oxidative stress on in vivo brain GSH turnover in young and mature mice. 氧化应激对年轻和成熟小鼠体内脑GSH转换的影响。

Molecular and chemical neuropathology Pub Date : 1997-04-01 DOI: 10.1007/BF02815097

M L Chang, L K Klaidman, J D Adams

{"title":"The effects of oxidative stress on in vivo brain GSH turnover in young and mature mice.","authors":"M L Chang, L K Klaidman, J D Adams","doi":"10.1007/BF02815097","DOIUrl":"https://doi.org/10.1007/BF02815097","url":null,"abstract":"Glutathione (GSH) synthetase activities and GSH turnover rates were examined during severe oxidative stress in the mouse brain as induced by t-butylhydroperoxide (t-BuOOH). Brain GSH synthetase activities in 8-mo-old mice in the cortex, striatum, thalamus, hippocampus, midbrain, and cerebellum were found to increase following t-BuOOH treatment. The effect of GSH synthesis on brain GSH turnover rates for 2- and 8-mo-old mice were determined after intracerebroventricular (icv) injection of [35S]cysteine. Rate constants for GSH turnover were determined by least-squares iterative minimization from the specific activity data from 20 min to 108 h after [35S]cysteine administration. GSH and glutathione disulfide (GSSG) specific activities were determined after separation by high-pressure liquid chromatography (HPLC). The half-life of GSH in the 2-mo-old mouse was 59.5 h and in the 8-mo-old mouse was 79.1 h. In summary, defense mechanisms against oxidative stress in the brain differ with age. Young mice can increase the cellular availability of GSH, whereas mature mice can increase GSH synthetase activity during oxidative stress. These differences make mature mice more susceptible to brain oxidative damage.","PeriodicalId":18736,"journal":{"name":"Molecular and chemical neuropathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02815097","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20112578","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 31

Morphochemical changes in brain structures in the course of chronic haloperidol treatment and the correction of these changes with tuftsin. 氟哌啶醇慢性治疗过程中脑结构的形态化学变化及氟哌啶醇对这些变化的纠正。

Molecular and chemical neuropathology Pub Date : 1997-04-01 DOI: 10.1007/BF02815099

L M Gershtein, M T Dobrynina, A V Sergutina

{"title":"Morphochemical changes in brain structures in the course of chronic haloperidol treatment and the correction of these changes with tuftsin.","authors":"L M Gershtein, M T Dobrynina, A V Sergutina","doi":"10.1007/BF02815099","DOIUrl":"https://doi.org/10.1007/BF02815099","url":null,"abstract":"The systemic injection of haloperidol (4 wk, 0.5 mg/kg/d) caused the increase of protein concentration and content, and the activity level of aminopeptidase in the cytoplasm of the neurons of associated type (layer III). The nucleus of these cells decreased both in sizes and in the content of proteins. In the neurons of efferent-projectory type (layer V), the decrease of studied peculiarities as compared with control level was observed. Tuftsin (300 micrograms/kg/d) injection after chronic haloperidol treatment causes the restoring action on changed parameters in sensomotor cortex. In caudate nucleus, tuftsin influence caused further reduction of neuron's cytoplasmic area and significant reduction in protein content. The received results testify to the morphobiochemical heterogenity of investigated brain structures, which is displayed both in the case of haloperidol treatment and in the case of its correction by neuropeptide tuftsin. Chronic haloperidol administration to animals can develop a model of certain symptoms and syndromes of parkinsonism. Its most pronounced manifestation is an imbalance in the neuromediator systems, especially the dopaminergic one (Mettler and Crandall, 1959; Colls, 1984; Funk et al., 1986). The research was performed in conjunction with the physiologists, whose experiments have shown that after chronic haloperidol administration, changes in animal behavior are developed that are typical for bradikinesia, and the motor regimen of integration is disturbed (Popova and Kachalova, 1991; Dovedova and Povova, 1993). Regulatory drugs, especially the tetrapeptide tuftsin, seem to correct such disturbances.","PeriodicalId":18736,"journal":{"name":"Molecular and chemical neuropathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02815099","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20112580","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Acrylamide and carbon disulfide treatments increase the rate of rat brain tubulin polymerization. 丙烯酰胺和二硫化碳处理增加了大鼠脑微管的聚合率。

Molecular and chemical neuropathology Pub Date : 1997-04-01 DOI: 10.1007/BF02815100

R P Gupta, M B Abou-Donia

{"title":"Acrylamide and carbon disulfide treatments increase the rate of rat brain tubulin polymerization.","authors":"R P Gupta, M B Abou-Donia","doi":"10.1007/BF02815100","DOIUrl":"https://doi.org/10.1007/BF02815100","url":null,"abstract":"Acrylamide and carbon disulfide produce central-peripheral distal axonopathy in experimental animals and humans. The main feature of this disease is the focal swellings containing neurofilaments in distal axons, followed by nerve degeneration beyond these swellings. We studied the possible role of tubulin assembly kinetics in this disease. The rats were either administered acrylamide (50 mg/kg, ip, saline) or exposed to carbon disulfide (700 ppm, 9 h) via inhalation for 12 and 15 d, respectively. Tubulin, purified from both acrylamide-(10.37 +/- 0.3 vs 11.3 +/- 0.15) and carbon disulfide-treated (9.72 +/- 0.5 vs 11.18 +/- 0.25) rat brains showed increase in Vmax (OD/min x 10(3)) of its polymerization. However, only acrylamide treatment showed a decrease in time to Vmax, when brain supernatant was used for tubulin polymerization. In vitro addition of acrylamide (0.1-1 mM) to bovine brain tubulin also showed a decrease in time to Vmax (16-21%) of its polymerization. Carbon disulfide treatment of rats, on the other hand, showed a decrease in MAP-2 and an increase in a 120-kDa peptide concentration. The latter showed immunoreactivity with anti-MAP-2. The increase in the rate of tubulin polymerization by acrylamide and carbon disulfide treatment may alter the rate of transport of axonal constituents, including neurofilament, and contribute toward their accumulation in the focal swellings observed in this neuropathy.","PeriodicalId":18736,"journal":{"name":"Molecular and chemical neuropathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02815100","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20112581","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 13

Retinoic acid synthesis in normal and Alzheimer diseased brain and human neural cells. 视黄酸在正常和阿尔茨海默病大脑和人类神经细胞中的合成。

Molecular and chemical neuropathology Pub Date : 1997-04-01 DOI: 10.1007/BF02815101

M J Connor, N Sidell

{"title":"Retinoic acid synthesis in normal and Alzheimer diseased brain and human neural cells.","authors":"M J Connor, N Sidell","doi":"10.1007/BF02815101","DOIUrl":"https://doi.org/10.1007/BF02815101","url":null,"abstract":"Retinoids play fundamental roles in CNS development, but their distribution, metabolism, and function within the mature human CNS are unknown. In these studies, extracts of autopsy tissues recovered from histopathologically confirmed control and Alzheimer diseased brains were tested for their ability to synthesize retinoic acid. Retinaldehyde dehydrogenase (RLDH), the enzyme that forms retinoic acid from retinaldehyde, was present in hippocampus, frontal cortex, and parietal cortex. The RLDH activity of hippocampus and parietal cortex from Alzheimer diseased brains was 1.5- to 2-fold higher (p < 0.05) compared to the controls. In contrast, the RLDH activity of frontal cortex was the same for both Alzheimer diseased and control groups. A cultured human glioblastoma (U251) and neuroblastoma (LA-N-5) cell line synthesized retinoic acid from retinaldehyde or retinol, suggesting that a variety of neural cell types possess this activity. LA-N-5 cells grown in vitamin A-depleted medium had higher (p < 0.05) RLDH activity (0.35 +/- 0.04 nmol/mg/h) than LA-N-5 cells grown in vitamin A-replete media (0.15 +/- 0.02 nmol/mg/h). This difference was lost when retinol was added back to the medium, confirming that a reduction in vitamin A supply can induce RLDH activity in neural cells. However, this feedback mechanism does not appear to explain the higher RLDH activity of Alzheimer diseased hippocampus and parietal cortex, because the overall vitamin A status as indicated by serum retinol and carotenoid levels and by hippocampal retinoid content was similar for the Alzheimer diseased and control groups. These studies establish the presence of retinoids and RLDH activity in human brain tissues, and indicate that retinoic acid synthesis is modulated in some regions of Alzheimer diseased brain.","PeriodicalId":18736,"journal":{"name":"Molecular and chemical neuropathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02815101","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20112426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 47

Granule cell mRNA levels for BDNF, NGF, and NT-3 correlate with neuron losses or supragranular mossy fiber sprouting in the chronically damaged and epileptic human hippocampus. BDNF、NGF和NT-3的颗粒细胞mRNA水平与慢性损伤和癫痫患者海马中神经元损失或颗粒上苔藓纤维发芽相关。

Molecular and chemical neuropathology Pub Date : 1997-01-01 DOI: 10.1007/BF02815150

G W Mathern, T L Babb, P E Micevych, C E Blanco, J K Pretorius

{"title":"Granule cell mRNA levels for BDNF, NGF, and NT-3 correlate with neuron losses or supragranular mossy fiber sprouting in the chronically damaged and epileptic human hippocampus.","authors":"G W Mathern, T L Babb, P E Micevych, C E Blanco, J K Pretorius","doi":"10.1007/BF02815150","DOIUrl":"https://doi.org/10.1007/BF02815150","url":null,"abstract":"This study determined in temporal lobe epilepsy patients if there were correlations among hippocampal granule cell expression of neurotrophin mRNAs, aberrant supragranular mossy fiber sprouting, and neuron losses. Consecutive surgically resected hippocampi (n = 9) and comparison tissue from autopsies (n = 3) were studied for: 1. Granule cell mRNA levels using in situ hybridization for brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and neurotrophin-3 (NT-3); 2. neo-Timm supragranular mossy fiber sprouting; and 3. Ammon's horn neuron densities. Clinically, patients were classified into those with hippocampal sclerosis (HS; n = 7) and non-HS cases (i.e., mass lesions and autopsies; n = 5). Results showed that compared to non-HS cases, HS patients showed increased granule cell mRNA levels for BDNF, NGF, and NT-3 (p = 0.035, p = 0.04, p = 0.045 respectively; one-tail directional test). Moreover, granule cell BDNF mRNA levels correlated inversely with Ammon's horn neuron densities (p = 0.02) and correlated positively with greater supragranular mossy fiber sprouting (p = 0.02). NGF mRNA levels correlated inversely with Ammon's horn neuron densities (p = 0.02), and NT-3 mRNA levels correlated inversely with age at surgery (p = 0.04) and correlated positively with greater mossy fiber sprouting (p = 0.026). These results indicate in the chronically damaged human hippocampus that granule cells express neurotrophin mRNAs, and mRNA levels correlate with either hippocampal neuron losses or aberrant supragranular mossy fiber sprouting. These data support the hypothesis that in the epileptic human hippocampus, there may be pathophysiologic associations among mossy fiber synaptic plasticity, hippocampal neuron damage, and granule cell mRNA neurotrophin levels.","PeriodicalId":18736,"journal":{"name":"Molecular and chemical neuropathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02815150","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20086652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 104

Limited junctional diversity of V delta 5-J delta 1 rearrangement in multiple sclerosis patients. 多发性硬化症患者V δ 5-J δ 1重排的有限连接多样性。

Molecular and chemical neuropathology Pub Date : 1997-01-01 DOI: 10.1007/BF02815152

J S Nowak, G Michałowska-Wender, D Januszkiewicz, M Wender

引用次数: 4

Inhibition of nitric oxide synthase potentiates hypertension and increases mortality in traumatically brain-injured rats. 抑制一氧化氮合酶可增强创伤性脑损伤大鼠的高血压并增加死亡率。

Molecular and chemical neuropathology Pub Date : 1997-01-01 DOI: 10.1007/BF02815154

Y C Lu, S Liu, Q Z Gong, R J Hamm, B G Lyeth

{"title":"Inhibition of nitric oxide synthase potentiates hypertension and increases mortality in traumatically brain-injured rats.","authors":"Y C Lu, S Liu, Q Z Gong, R J Hamm, B G Lyeth","doi":"10.1007/BF02815154","DOIUrl":"https://doi.org/10.1007/BF02815154","url":null,"abstract":"We examined the effects of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS), on mortality, morbidity, and cardiovascular parameters following traumatic brain injury (TBI) in the rat. Rats were anesthetized with 2% isoflurane prior to moderate (2.0 atmosphere), central fluid percussion TBI. Temporalis muscle temperature was maintained at 37 +/- 0.5 degrees C. L-NAME (10 mg/kg iv) was administered once at either 5 min before, 5 min after, or 15 min after TBI. Sensorimotor deficits and spatial learning/ memory deficits were assessed after injury. Separate groups of rats were monitored for cardiovascular parameters. Preinjury administration of L-NAME significantly increased mortality from 13 (vehicle) to 70% (associated with pulmonary edema), whereas postinjury, L-NAME had no effect on mortality (14 and 25%). L-NAME administered at 5 or 15 min after injury had no significant effect on motor performance or cognitive performance deficits associated with TBI. L-NAME in uninjured rats increased arterial blood pressure by 25 mmHg within 2 min. L-NAME injected 5 min before TBI greatly prolonged the hypertensive episode associated with TBI (1 min in vehicle vs 60 min in L-NAME). L-NAME injected 5 min after TBI caused a sustained 35 mmHg increase in blood pressure. These findings suggest that acute inhibition of NOS has detrimental consequences on mortality that may be owing to its cardiovascular effects.","PeriodicalId":18736,"journal":{"name":"Molecular and chemical neuropathology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1997-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02815154","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20086101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 38

Brain-derived neurotrophic factor suppresses programmed death of cerebellar granule cells through a posttranslational mechanism. 脑源性神经营养因子通过翻译后机制抑制小脑颗粒细胞程序性死亡。

Molecular and chemical neuropathology Pub Date : 1997-01-01 DOI: 10.1007/BF02815153

K Suzuki, T Koike

引用次数: 38