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Nervous system

About: Nervous system is a research topic. Over the lifetime, 16729 publications have been published within this topic receiving 847181 citations.


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Journal ArticleDOI
TL;DR: Data on the role of serotonin in learning and memory and on the effects of aging on brain serotonin function are reviewed and discussed in relation to pharmacologic treatment strategies for the memory impairments associated with advancing age.
Abstract: Serotonin is widely distributed throughout the central nervous system and is implicated in a variety of neural functions such as pain, feeding, sleep, sexual behavior, cardiac regulation and cognition. This paper is concerned with the last of these. Abnormalities of the serotonergic nervous system are well documented in pathologic studies of Alzheimer's disease and there is evidence suggesting that changes in this system occur in association with non-disease aging. Data on the role of serotonin in learning and memory and on the effects of aging on brain serotonin function are reviewed and discussed in relation to pharmacologic treatment strategies for the memory impairments associated with advancing age.

275 citations

Journal ArticleDOI
TL;DR: The timing and spatial distribution of Wnt-gene expression in the chick embryo further support the general hypothesis that Wnt genes play key roles in patterning the developing vertebrate nervous system.

274 citations

Journal ArticleDOI
TL;DR: The early transcription of F MR–1 gene and the distribution of FMR–1 mRNAs in human fetuses suggest that alterations of FMSG gene expression may contribute to the pathogenesis of fragile–X syndrome and especially the mental retardation.
Abstract: The expression of the FMR–1 gene, which is implicated in fragile–X syndrome was investigated in human fetuses by in situ hybridization. In 8 and 9 week–old fetuses, FMR–1 mRNAs are expressed in proliferating and migrating cells of the nervous system, in the retina, and in several non–nervous tissues. In the brain of 25 week–old fetuses, FMR–1 mRNAs are produced in all nearly differenciated structures, with the highest level in cholinergic neurons of the nucleus basalis magnocellularis and in pyramidal neurons of hippocampus. The early transcription of FMR–1 gene and the distribution of FMR–1 mRNAs in human fetuses suggest that alterations of FMR–1 gene expression may contribute to the pathogenesis of fragile–X syndrome and especially the mental retardation.

273 citations

Journal ArticleDOI
TL;DR: There is functional redundancy among the three KIF5s and that KIF3A and KIF4B prevented the KIF7C null mice from the severe phenotype, and three Kif5s showed high similarity in the amino acid sequence, could rescue the K IF5B mutant cells, and could form heterodimers.
Abstract: Kinesin superfamily proteins (KIFs) are the molecular motors conveying cargos along microtubules. KIF5s, the heavy chains of conventional kinesin (KHC), are originally identified members of KIFs, and neuronal KIF5A and ubiquitous KIF5B have been identified so far. In the present work, we cloned a novel member of KIF5, KIF5C, and generated specific antibodies against three KIF5s to investigate their distribution and functions. KIF5A showed pan-neuronal distribution in the nervous system. KIF5B showed a glial cell distribution pattern in general; however, interestingly, its expression was strongly upregulated in axon-elongating neurons, such as olfactory primary neurons and mossy fibers. KIF5C was also a neuronal KIF5 like KIF5A but was highly expressed in lower motor neurons in 2-week-old or older mice, suggesting its important roles in the maintenance of motor neurons rather than in their formation, such as axonal elongation. Because a large part of KIF5s in adult motor neurons were expected to be KIF5C, we generated mice lacking the kif5C gene to investigate the functions of KIF5C in neurons in living animals. The mutant mice showed smaller brain size but were viable and did not show gross changes in the nervous system. Closer examinations revealed the relative loss of motor neurons to sensory neurons. Because three KIF5s showed high similarity in the amino acid sequence, could rescue the KIF5B mutant cells, and could form heterodimers, we think that there are functional redundancy among the three KIF5s and that KIF5A and KIF5B prevented the KIF5C null mice from the severe phenotype.

273 citations

Journal ArticleDOI
TL;DR: The results raise the possibility that the NGF receptor has a role in the mechanism of NGF beyond the initial binding event at the plasma membrane of the axonal terminus.
Abstract: NGF acts on responsive neurons by binding to specific NGF receptors on axonal termini, after which a critical biochemical signal is retrogradely transported to the cell body. The identity of the signal(s) is unknown; candidates include NGF itself or some other "second messenger." A possible second messenger is the NGF receptor. As a first step in assessing the possible role of NGF receptor in the generation of the NGF-dependent signal, and in understanding the economy of NGF receptor synthesis and utilization, we determined whether the NGF receptor is retrogradely transported. Using immunohistochemical staining with a monoclonal antibody (192-IgG) against rat NGF receptor, we looked for accumulation of NGF receptor molecules distal (retrograde transport), as well as proximal (anterograde transport), to sites of axonal ligation or transection. By 10-12 hr in both the ligated sciatic nerve and the lesioned fimbria-fornix, accumulated NGF receptor was detected proximal and distal to the ligation/lesion site. The transported receptor presumably was located in sympathetic and sensory neurons in the sciatic nerve and in forebrain cholinergic neurons projecting from the medial septum to the hippocampus. In both anatomical sites, accumulation of NGF receptor on the proximal (anterograde) side occurred in streams of fine axonal processes, whereas staining on the distal (retrograde) side occurred in varicose or granular configurations. These results raise the possibility that the NGF receptor has a role in the mechanism of NGF beyond the initial binding event at the plasma membrane of the axonal terminus.

273 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023247
2022510
2021371
2020409
2019375
2018357