Clinical neuroscience (New York, N.Y.)最新文献_第10页

Molecular and cellular adaptations in signal transduction pathways following ethanol exposure. 乙醇暴露后信号转导途径中的分子和细胞适应性。

Clinical neuroscience (New York, N.Y.) Pub Date : 1995-01-01

L W Fitzgerald, E J Nestler

{"title":"Molecular and cellular adaptations in signal transduction pathways following ethanol exposure.","authors":"L W Fitzgerald, E J Nestler","doi":"","DOIUrl":"","url":null,"abstract":"The purpose of this review is to provide an overview of the acute actions of ethanol on signal transduction, as well as a selective consideration of some of the long-term adaptive changes in signal transduction pathways that may underlie clinical manifestations of ethanol dependence, tolerance, withdrawal, and addiction. The acute intoxicating effects of ethanol have been widely attributed to its ability to block voltage-gated Ca2+ and Na+ channels and N-methyl-D-aspartate glutamate receptor cation channels, and to facilitate GABAA receptor Cl- channels. Adaptive changes in these same proteins following chronic ethanol exposure may contribute to physical and psychological signs of ethanol dependence and withdrawal. Ethanol, as with other drugs of abuse, also acutely activates the mesolimbic dopamine pathway, an effect which likely accounts, at least in part, for ethanol's acute reinforcing properties. Studies directed at unraveling the biochemical and molecular basis of ethanol's acute and chronic actions may lead to the development of novel pharmacotherapeutics that mitigate aspects of acute ethanol intoxication and, more importantly, treat the effects of withdrawal and addiction (craving) associated with long-term ethanol abuse.","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"3 3","pages":"165-73"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19590785","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: 0

Amyotrophic lateral sclerosis and viruses. 肌萎缩侧索硬化症和病毒

Clinical neuroscience (New York, N.Y.) Pub Date : 1995-01-01

E F Salazar-Grueso, R P Roos

引用次数: 0

New diagnostic issues in schizophrenic disorders. 精神分裂症的新诊断问题。

Clinical neuroscience (New York, N.Y.) Pub Date : 1995-01-01

W T Carpenter, R W Buchanan, B Kirkpatrick

引用次数: 0

New morphological and neuropathological findings in schizophrenia: a neurodevelopmental perspective. 精神分裂症的形态学和神经病理学新发现:神经发育的观点。

Clinical neuroscience (New York, N.Y.) Pub Date : 1995-01-01

B G Bunney, S G Potkin, W E Bunney

{"title":"New morphological and neuropathological findings in schizophrenia: a neurodevelopmental perspective.","authors":"B G Bunney, S G Potkin, W E Bunney","doi":"","DOIUrl":"","url":null,"abstract":"This article reviews evidence for morphological abnormalities in schizophrenia as assessed by brain imaging and neurohistochemical techniques including immunohistochemistry and in situ hybridization. Localized deficits in schizophrenic brain appear in many regions including frontal and temporal lobes, anterior cingulate, mediodorsal thalamic nucleus, and corpus callosum. These areas are interconnected and may provide the basis for a \"psychosis circuitry.\" Neuronal disruption of elements in this circuitry may result in a hypothesized dysconnection syndrome. Evidence suggests an alteration in neuronal development related to either genetic and/or environmental factors. Primary and secondary anterograde and retrograde effects may accompany this neurodevelopmental defect and may further alter intrinsic and extrinsic neuronal communications. A number of studies are consistent with the second trimester of gestation being a critical period for fetal brain development, especially for neuronal migration. Fetal trauma due to environmental insults (e.g., influenza) during this trimester may increase the incidence of schizophrenia. Recent advances in the identification of factors that modulate neuronal development including axon guidance molecules, neurotrophins, and programmed cell death genes provide intriguing new areas for potential investigation. Future research may focus on the factors controlling neuronal migration and programmed cell death in the schizophrenic brain.","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"3 2","pages":"81-8"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18589382","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: 0

The genetic basis of ataxia. 共济失调的遗传基础。

Clinical neuroscience (New York, N.Y.) Pub Date : 1995-01-01

R N Rosenberg

引用次数: 0

Schizophrenia: a disconnection syndrome? 精神分裂症:一种脱节综合症?

Clinical neuroscience (New York, N.Y.) Pub Date : 1995-01-01

K J Friston, C D Frith

引用次数: 0

Dentatorubral-pallidoluysian atrophy (DRPLA). Molecular basis for wide clinical features of DRPLA. 齿状体-白斑萎缩(DRPLA)。DRPLA广泛临床特征的分子基础。

Clinical neuroscience (New York, N.Y.) Pub Date : 1995-01-01

T Ikeuchi, R Koide, O Onodera, H Tanaka, M Oyake, H Takano, S Tsuji

{"title":"Dentatorubral-pallidoluysian atrophy (DRPLA). Molecular basis for wide clinical features of DRPLA.","authors":"T Ikeuchi, R Koide, O Onodera, H Tanaka, M Oyake, H Takano, S Tsuji","doi":"","DOIUrl":"","url":null,"abstract":"Dentatorubral-pallidoluysian atrophy (DRPLA) is a rare autosomal dominant neurodegenerative disorder characterized clinically by various combinations of myoclonus, epilepsy, cerebellar ataxia, choreoathetosis, dementia and psychiatric symptoms. Based on the phenomenon of anticipation, the gene for DRPLA was recently identified. DRPLA is caused by unstable expansion of a CAG repeat in the gene located on the short arm of chromosome 12. As have been observed in Huntington's disease and SCA1, there is a strong correlation between the age of onset and the size of CAG repeats. Furthermore, patients with larger repeats tend to show a PME (progressive myoclonus epilepsy) phenotype as well as earlier ages of onset. More prominent anticipation and larger intergenerational increase of CAG repeats in paternal transmission can be accounted for by the meiotic instability of CAG repeats in male gametogenesis. Comparison of size distributions of CAG repeats in Japanese, African-American and white populations revealed that 7.4% of the Japanese alleles had greater than 19 repeats, whereas none of the whites and 1% of the African-American alleles were of this size. The results may account for the ethnic predilection of DRPLA.","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"3 1","pages":"23-7"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18618935","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: 0

Friedreich's ataxia-vitamin E responsive type. The chromosome 8 locus. 弗里德赖希的共济失调-维生素E反应型。染色体8位点。

Clinical neuroscience (New York, N.Y.) Pub Date : 1995-01-01

S Belal, F Hentati, C Ben Hamida, M Ben Hamida

引用次数: 0

Genetics of myoclonic and myoclonus epilepsies. 肌阵挛性和肌阵挛性癫痫的遗传学。

Clinical neuroscience (New York, N.Y.) Pub Date : 1995-01-01

B A Minassian, J Sainz, A V Delgado-Escueta

{"title":"Genetics of myoclonic and myoclonus epilepsies.","authors":"B A Minassian, J Sainz, A V Delgado-Escueta","doi":"","DOIUrl":"","url":null,"abstract":"Mendelian forms of benign myoclonic epilepsies where a chromosomal locus has been defined include (1) the autosomal dominant (AD) juvenile myoclonic epilepsy (JME) in chr. 6p11, (2) the autosomal dominant childhood absence epilepsy which evolves to JME in chr. 1p, (3) familial adult myoclonic epilepsy of Yasuda and Inazuki, and (4) possibly JME within the idiopathic generalized epilepsy susceptibility gene in chr. 8 reported by Zara et al (1995). Other myoclonic epilepsy syndromes with onset in the first year of life (Aicardi's Neonatal (Early) Myoclonic Encephalopathy, West's Syndrome, Dravet's Severe Myoclonic Epilepsy, and Dravet's Benign Myoclonic Epilepsy of Infancy), in early childhood (Lennox-Gastaut-Dravet Syndrome, Myoclonic Variant of Lennox Gastaut Dravet Syndrome, Myoclonic-Astatic Epilepsy of Doose, Benign Myoclonic Epilepsies (BME), or even in late childhood (Childhood Absence Epilepsy with myoclonias, vs. Myoclonic Absence Epilepsy) are probably genetically complex diseases. Amongst the progressive myoclonus epilepsy syndromes, specific mutations have already been defined in Unverricht Lundborg disease, ceroid lipofuscinoses 3 or Spielmayer Voight syndrome within Battens disease, sialidosis, dentadorubropallidoluysian atrophy and the mitochondrial syndrome MERRF. Most recently our laboratories established the locus for Lafora's disease in chr. 6q and results are speedily moving towards the definition of its mutation.","PeriodicalId":79395,"journal":{"name":"Clinical neuroscience (New York, N.Y.)","volume":"3 4","pages":"223-35"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19856904","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: 0

Adenovirus for neurodegenerative diseases: in vivo strategies and ex vivo gene therapy using human neural progenitors. 腺病毒治疗神经退行性疾病:体内策略和体外基因治疗使用人类神经祖细胞。

Clinical neuroscience (New York, N.Y.) Pub Date : 1995-01-01

O Sabaté, M Barkats, M H Buc-Caron, M N Castel-Barthe, F Finiels, P Horellou, F Revah, J Mallet

引用次数: 0