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Learning to perform a behavioural procedure as a well-ingrained habit requires extensive repetition of the behavioural sequence, and learning not to perform such behaviours is notoriously difficult. Yet regaining a habit can occur quickly, with even one or a few exposures to cues previously triggering the behaviour. To identify neural mechanisms that might underlie such learning dynamics, we made long-term recordings from multiple neurons in the sensorimotor striatum, a basal ganglia structure implicated in habit formation, in rats successively trained on a reward-based procedural task, given extinction training and then given reacquisition training. The spike activity of striatal output neurons, nodal points in cortico-basal ganglia circuits, changed markedly across multiple dimensions during each of these phases of learning. First, new patterns of task-related ensemble firing successively formed, reversed and then re-emerged. Second, task-irrelevant firing was suppressed, then rebounded, and then was suppressed again. These changing spike activity patterns were highly correlated with changes in behavioural performance. We propose that these changes in task representation in cortico-basal ganglia circuits represent neural equivalents of the explore-exploit behaviour characteristic of habit learning. 相似文献
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Riassunto Si dimostra che l'utero di ratta, sottoposta ad ablazione della ovaie 15 mesi e mezzo prima, risponde nettamente a tre iniezioni sottocutanee quotidiane di 17-estradiolo: si ottennero aumenti di peso del 92, 207 e 231% al di sopra del peso degli uteri di controlli sottoposti ad ovariectomia e trattati con semplice olio di sesamo. Si conclude, percio, che l'utero di ratta esposta a deficienza ormonica ovarica di lunga durata è notevolmente sensibile a trattamento con estrogeni. 相似文献
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E. Katchburian Ann M. C. Burgess F. R. Johnson 《Cellular and molecular life sciences : CMLS》1973,29(8):1020-1022
Résumé A l'aide du microscope électronique muni d'un goniomètre, la structure tri-dimensionelle du disque Z de la fibre musculaire striée a été analysée. Les résultats obtenus sont comparés avec un modèle construit en perspex et avec les images conventionnelles du disque Z.
Acknowledgment. We wish to thank Pye Unicam (Philips) an Jeol (U. K.) Ltd. for kindly allowing us to use their electron microscopes. Technical assistance from Messrs.H. Fisher, J. Manston andR. Birchenough is gratefully acknowledged. 相似文献
Acknowledgment. We wish to thank Pye Unicam (Philips) an Jeol (U. K.) Ltd. for kindly allowing us to use their electron microscopes. Technical assistance from Messrs.H. Fisher, J. Manston andR. Birchenough is gratefully acknowledged. 相似文献
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Crow YJ Hayward BE Parmar R Robins P Leitch A Ali M Black DN van Bokhoven H Brunner HG Hamel BC Corry PC Cowan FM Frints SG Klepper J Livingston JH Lynch SA Massey RF Meritet JF Michaud JL Ponsot G Voit T Lebon P Bonthron DT Jackson AP Barnes DE Lindahl T 《Nature genetics》2006,38(8):917-920
Aicardi-Goutières syndrome (AGS) presents as a severe neurological brain disease and is a genetic mimic of the sequelae of transplacentally acquired viral infection. Evidence exists for a perturbation of innate immunity as a primary pathogenic event in the disease phenotype. Here, we show that TREX1, encoding the major mammalian 3' --> 5' DNA exonuclease, is the AGS1 gene, and AGS-causing mutations result in abrogation of TREX1 enzyme activity. Similar loss of function in the Trex1(-/-) mouse leads to an inflammatory phenotype. Our findings suggest an unanticipated role for TREX1 in processing or clearing anomalous DNA structures, failure of which results in the triggering of an abnormal innate immune response. 相似文献