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Neuropeptides in the autonomic nervous system. 自主神经系统中的神经肽。
CRC critical reviews in clinical neurobiology Pub Date : 1985-01-01
P Marley, B G Livett
{"title":"Neuropeptides in the autonomic nervous system.","authors":"P Marley,&nbsp;B G Livett","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This review will concern itself with recent advances in our knowledge about the anatomy, cellular distribution, and proposed function of neuropeptides in the peripheral nervous system. In particular, the concept of co-storage and co-release of neuropeptides with conventional neurotransmitters will be dealt with in regard to their known distribution in the three broad divisions of the autonomic nervous system: sensory neurons, autonomic neurons, and the adrenal medulla. The proposed physiological functions of the peptides in these three systems will be reviewed.</p>","PeriodicalId":77841,"journal":{"name":"CRC critical reviews in clinical neurobiology","volume":"1 3","pages":"201-83"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"15030319","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
Alzheimer's disease and related dementias: selective involvement of specific neuronal systems. 阿尔茨海默病和相关痴呆:特定神经元系统的选择性参与。
CRC critical reviews in clinical neurobiology Pub Date : 1985-01-01
P J Whitehouse, R G Struble, J C Hedreen, A W Clark, D L Price
{"title":"Alzheimer's disease and related dementias: selective involvement of specific neuronal systems.","authors":"P J Whitehouse,&nbsp;R G Struble,&nbsp;J C Hedreen,&nbsp;A W Clark,&nbsp;D L Price","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The brains of individuals with dementia due to Alzheimer's disease (AD), Parkinson's disease (PD), and Down's syndrome (DS) exhibit similar neuropathological features, including neuritic plaques, neurofibrillary tangles, and the loss of specific populations of neurons. In addition, these brains show similar transmitter-specific neurochemical alterations. Recent evidence indicates that several pathological and neurochemical changes are related to diseases involving projection systems innervating the telencephalon. At least two transmitter-specific circuits, cholinergic neurons in the basal forebrain and noradrenergic neurons in the locus coeruleus, are selectively affected in many patients with these disorders. This review focuses on these systems because they provide particularly useful examples of the ways in which multidisciplinary studies can provide new clinical-pathological-chemical correlations. Strategies used in these studies are applicable to a wide variety of other neurodegenerative diseases affecting specific populations of neurons. Modern neuropathological approaches to these diseases should eventually allow investigators to directly relate pathogenic processes involving transmitter-specific neuronal populations, whose projections, physiological properties, and functions are known, with the clinical manifestations occurring in human disorders of behavior and cognition.</p>","PeriodicalId":77841,"journal":{"name":"CRC critical reviews in clinical neurobiology","volume":"1 4","pages":"319-39"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"14011960","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
Prions--infectious pathogens causing the spongiform encephalopathies. 朊病毒——引起海绵状脑病的传染性病原体。
CRC critical reviews in clinical neurobiology Pub Date : 1985-01-01
S B Prusiner, D T Kingsbury
{"title":"Prions--infectious pathogens causing the spongiform encephalopathies.","authors":"S B Prusiner,&nbsp;D T Kingsbury","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The novel properties of the scrapie and Creutzfeldt-Jakob disease (CJD) transmissible agents readily distinguish them from viruses and viroids; thus, they have been labeled \"prions\". The scrapie prion contains a protein(s) which is required for infectivity; recently a 27,000 to 30,000 MW protein which purifies with the prion has been identified. The similarities between the scrapie and CJD agents suggest that CJD is also caused by a prion. Recent studies show that the time courses of both scrapie and CJD are determined by an autosominal dominant gene denoted PID (prion incubation determinant). In congenic mice infected with CJD, PID appears to be located on chromosome 17 in the major histocompatibility complex (H-2) in the D-subregion. Further studies indicate that replication of the scrapie and CJD prions precedes the development of pathological change. These changes share many similarities with those found in a variety of degenerative neurological disorders of unknown etiology.</p>","PeriodicalId":77841,"journal":{"name":"CRC critical reviews in clinical neurobiology","volume":"1 3","pages":"181-200"},"PeriodicalIF":0.0,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"15028497","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
Disorders of glycogen metabolism of muscle. 肌肉糖原代谢紊乱。
CRC critical reviews in clinical neurobiology Pub Date : 1984-01-01
S DiMauro, N Bresolin, A P Hays
{"title":"Disorders of glycogen metabolism of muscle.","authors":"S DiMauro,&nbsp;N Bresolin,&nbsp;A P Hays","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This review will briefly outline the major steps of glycogen metabolism in muscle and the role of glycogen as a source of energy in different types of exercise. There are nine specific enzyme defects of glycogen metabolism or glycolysis affecting muscle. Each of the nine glycogenoses will be discussed in terms of typical and variant clinical presentation, genetic transmission, muscle biopsy and biochemical findings. The proposed pathophysiology of the various symptoms and signs will be presented and the many unsolved problems in this area will be discussed.</p>","PeriodicalId":77841,"journal":{"name":"CRC critical reviews in clinical neurobiology","volume":"1 2","pages":"83-116"},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17307119","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
Scientific approaches to Huntington's disease. 亨廷顿舞蹈症的科学方法。
CRC critical reviews in clinical neurobiology Pub Date : 1984-01-01
P R Sanberg, J T Coyle
{"title":"Scientific approaches to Huntington's disease.","authors":"P R Sanberg,&nbsp;J T Coyle","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Huntington's Disease (HD) is a progressive neurologic disorder transmitted as autosomal dominant. The symptoms of HD, which typically appear in midlife, include disturbances in movement, psychiatric symptoms, and a progressive dementia. Neuropathologic studies indicate a distinct pattern of neuronal degeneration in HD that affects many areas of the brain but consistently and severely involves the basal ganglia including the caudate, putamen, and globus pallidus. The basal ganglia undergo a progressive atrophy due to degeneration of intrinsic neurons that results in ventricular enlargement. Over the last decade, detailed neurochemical analyses have been carried out on the brains of patients who have died with HD. These studies have demonstrated the selective degeneration of chemically defined neuronal systems including the striatal cholinergic intrinsic neurons, the striatal nigral GABAergic pathway, and striatal peptidergic neurons with the relative sparing of other systems such as the nigrostriatal pathway. These findings have resulted in a better understanding of the pathophysiologic basis for the movement disorder of HD and have led to the development of pharmacologic strategies to correct the synaptic neurochemical imbalances. Recent studies have begun to focus on mechanisms responsible for the selective neuronal degeneration in HD. One promising hypothesis evolved from the finding that intrastriatal injections of excitatory amino acid analogues reproduces the neurochemical and histologic pathology of HD in experimental animals; as a consequence, it has been hypothesized that dysfunction of excitatory amino acid neurotransmission may cause the selective neuronal degeneration of HD. Another hypothesis involves an abnormality of the plasma membrane based upon observations of differences in membrane characteristics in fibroblasts and red blood cells from HD patients as compared to suitable controls. The ultimate goals of these studies are to develop methods for identifying presymptomatic carriers of the HD gene as well as strategies for preventing the neuronal degeneration associated with expression of the gene.</p>","PeriodicalId":77841,"journal":{"name":"CRC critical reviews in clinical neurobiology","volume":"1 1","pages":"1-44"},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17167531","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
Stuttering. 口吃。
CRC critical reviews in clinical neurobiology Pub Date : 1984-01-01
D B Rosenfield
{"title":"Stuttering.","authors":"D B Rosenfield","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Stuttering has been with us throughout time. It is global, pan-cultural, and is noted in all languages. Of the adult population, 1-2% stutter; 4% of children stutter. Any theory purporting to explain stuttering must explain the co-contraction of laryngeal agonist and antagonists, genetic findings of stuttering, the male sexual bias, and the fluency evoking paradigms of singing, speaking while inhaling, white noise, and delayed auditory feedback. This paper presents a neuro-laryngeal analysis of stuttering that attempts to correlate these phenomena. Various neurophysiologic mechanisms of cerebral/laryngeal/auditory systems will be discussed.</p>","PeriodicalId":77841,"journal":{"name":"CRC critical reviews in clinical neurobiology","volume":"1 2","pages":"117-39"},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17459761","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
Studies of autoimmunity in multiple sclerosis. 多发性硬化症自身免疫的研究。
CRC critical reviews in clinical neurobiology Pub Date : 1984-01-01
J N Whitaker, D S Snyder
{"title":"Studies of autoimmunity in multiple sclerosis.","authors":"J N Whitaker,&nbsp;D S Snyder","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The central nervous system myelin unit (the myelin sheath and the supporting oligodendrocyte) may be damaged by a number of immune-mediated mechanisms involving cellular or humoral factors. In this review the following areas will be considered: the composition and properties of central nervous system myelin, the chemical and biological characteristics of oligodendrocytes, the participation of the central nervous system myelin unit in experimentally induced diseases, and a description and analysis of immunological abnormalities in humans with multiple sclerosis.</p>","PeriodicalId":77841,"journal":{"name":"CRC critical reviews in clinical neurobiology","volume":"1 1","pages":"45-82"},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17459760","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
Motoneuron death in the embryo. 胚胎中的运动神经元死亡。
CRC critical reviews in clinical neurobiology Pub Date : 1984-01-01
A H Lamb
{"title":"Motoneuron death in the embryo.","authors":"A H Lamb","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In the developing embryo, 50% or more of the young motoneurons supplying the limb die. Amputation studies suggest that motoneurons depend on acquiring trophic factors from the limb. However, access to the trophic factors is under complex control since all motoneurons, whether destined to live or die, send axons into the limb. Axon invasion is not random but under the control of an axon guidance mechanism. Motoneurons probably compete for access to trophic factors at the neuromuscular junction. In order to compete, the motor axons must first be guided to specific limb regions. Failure causes death. Recent evidence suggests that motoneurons are specified for small localities within individual muscles and that the failure rate may be high enough to account for a large proportion of motoneuron deaths. The mechanisms of the implied recognition between motoneurons and muscles are unknown but may depend on positionally determined cell surface markers, histochemical compatibility, and functional congruence.</p>","PeriodicalId":77841,"journal":{"name":"CRC critical reviews in clinical neurobiology","volume":"1 2","pages":"141-79"},"PeriodicalIF":0.0,"publicationDate":"1984-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17167374","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
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