Synapsin
Mostrando 1-12 de 64 artigos, teses e dissertações.
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1. Possible roles of COX-1 in learning and memory impairment induced by traumatic brain injury in mice
People who suffer from traumatic brain injury (TBI) often experience cognitive deficits in spatial reference and working memory. The possible roles of cyclooxygenase-1 (COX-1) in learning and memory impairment in mice with TBI are far from well known. Adult mice subjected to TBI were treated with the COX-1 selective inhibitor SC560. Performance in the open f
Braz J Med Biol Res. Publicado em: 16/09/2014
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2. The central nervous system as target for anti-hypertensive actions of a proline-rich peptide from Bothrops jararaca venom / O sistema nervoso central como alvo das ações anti-hipertensivas de um peptídeo rico em resíduo de prolina do veneno da Bothrops jararaca
Os peptídeos potenciadores da bradicinina (BPPs) presentes no veneno da serpente Bothrops jararaca são oligopeptídeos ricos em prolinas. Eles foram os primeiros inibidores naturais da enzima conversora de angiotensina (ECA) descritos. As propriedades bioquímicas e farmacológicas desses peptídeos foram essenciais para o desenvolvimento do captopril, o p
Publicado em: 2009
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3. A third member of the synapsin gene family
Synapsins are a family of neuron-specific synaptic vesicle-associated phosphoproteins that have been implicated in synaptogenesis and in the modulation of neurotransmitter release. In mammals, distinct genes for synapsins I and II have been identified, each of which gives rise to two alternatively spliced isoforms. We have now cloned and characterized a thir
The National Academy of Sciences.
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4. Norepinephrine and isoproterenol increase the phosphorylation of synapsin I and synapsin II in dentate slices of young but not aged Fisher 344 rats.
A number of recent reports have suggested that norepinephrine (NE) produces a form of synaptic enhancement that resembles long-term potentiation (LTP). LTP, thought to be an electrophysiological correlate of memory, in part involves an augmentation of transmitter release. Although the effects of NE have not been unequivocally linked to LTP, it is clear that
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5. Cytosolic rat brain synapsin I is a diacylglycerol kinase.
The phosphorylation of diacylglycerol (DG), a reaction catalyzed by DG kinase, may be critical in the termination of effector-induced signals mediated by protein kinase C. Synapsin I is a principal target of intracellular protein kinases and is thought to be involved in the release of neurotransmitter from axon terminals. We present several lines of evidence
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6. Synapsin I interacts with c-Src and stimulates its tyrosine kinase activity
Synapsin I is a synaptic vesicle-associated phosphoprotein that has been implicated in the formation of presynaptic specializations and in the regulation of neurotransmitter release. The nonreceptor tyrosine kinase c-Src is enriched on synaptic vesicles, where it accounts for most of the vesicle-associated tyrosine kinase activity. Using overlay, affinity ch
The National Academy of Sciences of the USA.
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7. Translocation of synapsin I in response to depolarization of isolated nerve terminals.
Depolarization of isolated nerve terminals (synaptosomes) has been shown to stimulate neurotransmitter release and to increase the phosphorylation state of a number of proteins, including synapsin I, in a Ca2+-dependent manner. Synapsin I, a prominent nerve terminal phosphoprotein, interacts with the cytoplasmic surface of small synaptic vesicles and with cy
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8. Synaptic targeting domains of synapsin I revealed by transgenic expression in photoreceptor cells.
Synapsins are abundant nerve terminal proteins present at all synapses except for ribbon synapses, e.g. photoreceptor cell synapses. Multiple functions have been proposed for synapsins, including clustering of synaptic vesicles and regulation of synaptic vesicle exocytosis. To investigate the physiological functions of synapsin and to ascertain which domains
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9. Molecular cloning of cDNAs for the nerve-cell specific phosphoprotein, synapsin I.
To provide access to synapsin I-specific DNA sequences, we have constructed cDNA clones complementary to synapsin I mRNA isolated from rat brain. Synapsin I mRNA was specifically enriched by immunoadsorption of polysomes prepared from the brains of 10-14 day old rats. Employing this enriched mRNA, a cDNA library was constructed in pBR322 and screened by diff
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10. Impairment of synaptic vesicle clustering and of synaptic transmission, and increased seizure propensity, in synapsin I-deficient mice.
Synapsin I has been proposed to be involved in the modulation of neurotransmitter release by controlling the availability of synaptic vesicles for exocytosis. To further understand the role of synapsin I in the function of adult nerve terminals, we studied synapsin I-deficient mice generated by homologous recombination. The organization of synaptic vesicles
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11. Kinetic analysis of the phosphorylation-dependent interactions of synapsin I with rat brain synaptic vesicles.
1. Synapsin I, a major synaptic vesicle (SV)-associated phosphoprotein, is involved in the regulation of neurotransmitter release and synapse formation. By binding to both phospholipid and protein components of SV with high affinity and in a phosphorylation-dependent fashion, synapsin I is believed to cluster SV and to attach them to the actin-based cytoskel
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12. Impairment of axonal development and of synaptogenesis in hippocampal neurons of synapsin I-deficient mice.
Synapsin I, the most abundant of all neuronal phosphoproteins, is enriched in synaptic vesicles. It has been hypothesized to regulate synaptogenesis and neurotransmitter release from adult nerve terminals. The evidence for such roles has been highly suggestive but not compelling. To evaluate the possible involvement of synapsin I in synaptogenesis and in the