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  • 1
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    Reversal and stabilization of synaptic modifications in a developing visual system (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-06-21
    Description: Persistent synaptic modifications are essential for experience-dependent refinement of developing circuits. However, in the developing Xenopus retinotectal system, activity-induced synaptic modifications were quickly reversed either by subsequent spontaneous activity in the tectum or by exposure to random visual inputs. This reversal depended on the burst spiking and activation of the N-methyl-D-aspartate subtype of glutamate receptors. Stabilization of synaptic modifications can be achieved by an appropriately spaced pattern of induction stimuli. These findings underscore the vulnerable nature of activity-induced synaptic modifications in vivo and suggest a temporal constraint on the pattern of visual inputs for effective induction of stable synaptic modifications.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhou, Qiang -- Tao, Huizhong W -- Poo, Mu-ming -- NS 36999/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2003 Jun 20;300(5627):1953-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurobiology, Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720-3200, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12817152" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Long-Term Potentiation ; Long-Term Synaptic Depression ; Neurons/physiology ; Okadaic Acid/pharmacology ; Patch-Clamp Techniques ; Phosphoprotein Phosphatases/antagonists & inhibitors/metabolism ; Photic Stimulation ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/physiology ; Retina/growth & development/*physiology ; Retinal Ganglion Cells/*physiology ; Superior Colliculi/cytology/growth & development/*physiology ; Synapses/*physiology ; Synaptic Transmission ; *Vision, Ocular ; Visual Pathways/growth & development/*physiology ; Xenopus
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Fine-tuning of pre-balanced excitation and inhibition during auditory cortical development (2010)
    Nature Publishing Group (NPG)
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    Publication Date: 2010-06-19
    Description: Functional receptive fields of neurons in sensory cortices undergo progressive refinement during development. Such refinement may be attributed to the pruning of non-optimal excitatory inputs, reshaping of the excitatory tuning profile through modifying the strengths of individual inputs, or strengthening of cortical inhibition. These models have not been directly tested because of the technical difficulties in assaying the spatiotemporal patterns of functional synaptic inputs during development. Here we apply in vivo whole-cell voltage-clamp recordings to the recipient layer 4 neurons in the rat primary auditory cortex (A1) to determine the developmental changes in the frequency-intensity tonal receptive fields (TRFs) of their excitatory and inhibitory inputs. Surprisingly, we observe co-tuned excitation and inhibition immediately after the onset of hearing, suggesting that a tripartite thalamocortical circuit with relatively strong feedforward inhibition is formed independently of auditory experience. The frequency ranges of tone-driven excitatory and inhibitory inputs first expand within a few days of the onset of hearing and then persist into adulthood. The latter phase is accompanied by a sharpening of the excitatory but not inhibitory frequency tuning profile, which results in relatively broader inhibitory tuning in adult A1 neurons. Thus the development of cortical synaptic TRFs after the onset of hearing is marked by a slight breakdown of previously formed excitation-inhibition balance. Our results suggest that functional refinement of cortical TRFs does not require a selective pruning of inputs, but may depend more on a fine adjustment of excitatory input strengths.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909826/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909826/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sun, Yujiao J -- Wu, Guangying K -- Liu, Bao-Hua -- Li, Pingyang -- Zhou, Mu -- Xiao, Zhongju -- Tao, Huizhong W -- Zhang, Li I -- EY018718/EY/NEI NIH HHS/ -- EY019049/EY/NEI NIH HHS/ -- R01 DC008983/DC/NIDCD NIH HHS/ -- R01 DC008983-01/DC/NIDCD NIH HHS/ -- R01 DC008983-02/DC/NIDCD NIH HHS/ -- R01 DC008983-03/DC/NIDCD NIH HHS/ -- R01 DC008983-04/DC/NIDCD NIH HHS/ -- R01 EY019049/EY/NEI NIH HHS/ -- R01 EY019049-02/EY/NEI NIH HHS/ -- R01DC008983/DC/NIDCD NIH HHS/ -- R03 DC006814/DC/NIDCD NIH HHS/ -- R03 DC006814-01A1/DC/NIDCD NIH HHS/ -- R03 DC006814-02/DC/NIDCD NIH HHS/ -- R03 DC006814-03/DC/NIDCD NIH HHS/ -- R21 DC008588/DC/NIDCD NIH HHS/ -- R21 DC008588-01/DC/NIDCD NIH HHS/ -- R21 DC008588-02/DC/NIDCD NIH HHS/ -- R21DC008588/DC/NIDCD NIH HHS/ -- UL1 RR025755/RR/NCRR NIH HHS/ -- England -- Nature. 2010 Jun 17;465(7300):927-31. doi: 10.1038/nature09079.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, California 90089, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20559386" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustic Stimulation ; Animals ; Auditory Cortex/growth & development/*physiology ; Auditory Pathways/physiology ; Electrical Synapses/physiology ; Excitatory Postsynaptic Potentials/*physiology ; Hearing/physiology ; Neural Inhibition/*physiology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Sensory Receptor Cells/*physiology ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Transcriptional repressor REST drives lineage stage-specific chromatin compaction at Ptch1 and increases AKT activation in a mouse model of medulloblastoma (2019)
    The American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2019
    Description: 〈p〉In medulloblastomas (MBs), the expression and activity of RE1-silencing transcription factor (REST) is increased in tumors driven by the sonic hedgehog (SHH) pathway, specifically the SHH-α (children 3 to 16 years) and SHH-β (infants) subgroups. Neuronal maturation is greater in SHH-β than SHH-α tumors, but both correlate with poor overall patient survival. We studied the contribution of REST to MB using a transgenic mouse model (〈i〉RESTTG〈/i〉〈sup〉〈/sup〉) wherein conditional 〈i〉NeuroD2〈/i〉-controlled 〈i〉REST〈/i〉 transgene expression in lineage-committed 〈i〉Ptch1〈/i〉〈sup〉+/–〈/sup〉 cerebellar granule neuron progenitors (CGNPs) accelerated tumorigenesis and increased penetrance and infiltrative disease. This model revealed a neuronal maturation context–specific antagonistic interplay between the transcriptional repressor REST and the activator GLI1 at 〈i〉Ptch1〈/i〉. Expression of 〈i〉Arrb1〈/i〉, which encodes β-arrestin1 (a GLI1 inhibitor), was substantially reduced in proliferating and, to a lesser extent, lineage-committed 〈i〉RESTTG〈/i〉〈sup〉〈/sup〉 cells compared with wild-type proliferating CGNPs. Lineage-committed 〈i〉REST〈sup〉TG〈/sup〉〈/i〉 cells also had decreased GLI1 activity and increased histone H3K9 methylation at the 〈i〉Ptch1〈/i〉 locus, which correlated with premature silencing of 〈i〉Ptch1〈/i〉. These cells also had decreased expression of 〈i〉Pten〈/i〉, which encodes a negative regulator of the kinase AKT. Expression of 〈i〉PTCH1〈/i〉 and 〈i〉GLI1〈/i〉 were less, and 〈i〉ARRB1〈/i〉 was somewhat greater, in patient SHH-β than SHH-α MBs, whereas that of 〈i〉PTEN〈/i〉 was similarly lower in both subtypes than in others. Inhibition of histone modifiers or AKT reduced proliferation and induced apoptosis, respectively, in cultured REST-high MB cells. Our findings linking REST to differentiation-specific chromatin remodeling, 〈i〉PTCH1〈/i〉 silencing, and AKT activation in MB tissues reveal potential subgroup-specific therapeutic targets for MB patients.〈/p〉
    Print ISSN: 1945-0877
    Electronic ISSN: 1937-9145
    Topics: Biology , Medicine
    Published by The American Association for the Advancement of Science (AAAS)
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  • 4
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    Retrograde signaling at central synapses (2001)
    National Academy of Sciences
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    Publication Date: 2001-09-25
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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