Mechanisms for regulating synaptic efficiency in the visual cortex |
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| Affiliation: | 1. Service de Neurologie, CHU de Bordeaux, F-33076 Bordeaux, France;2. Department of Neurology, Sahlgrenska University Hospital, 413 45 Göteborg, Sweden;3. Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston;4. Institute of Brain Behaviour and Mental Heath, University of Manchester, UK;5. Institute of Clinical Neurobiology, Kenyongasse 18, A-1070 Vienna, Austria;6. Quanterix, Inc., Lexington, MA 021421, USA;7. Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria;8. Paracelsus-Elena-Klinik, Kassel, Germany and Department of Neuropathology, University Medical Center Goettingen, Germany;9. Program in Neuroscience, The Ottawa Hospital, University of Ottawa Brain and Mind Research Institute, Ottawa, Ontario, Canada;10. Perelman School of Medicine, University of Pennsylvania;11. Department of Neurology, Parkinson Center, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre, Nijmegen, the Netherlands;12. Department of Laboratory Medicine, Parkinson Center, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Centre, Nijmegen, the Netherlands;13. Department of Neurology, Bispebjerg University Hospital, Copenhagen, Denmark;14. Department of Pathology, University of WA, Seattle, USA;15. Centre de référence atrophie multisystématisée, CHU de Bordeaux, F-33076 Bordeaux, France;p. Univ. de Bordeaux, Institut des Maladies Neurodégénératives, UMR 5293, F-33076 Bordeaux, France;q. CNRS, Institut des Maladies Neurodégénératives, UMR 5293, F-33076 Bordeaux, France;1. Center for Magnetic Resonance Research (CMRR), University of Minnesota, MN 55455, United States;2. Department of Radiology, University of Minnesota, MN 55455, United States;3. Department of Neuroscience, University of Minnesota, MN 55455, United States;4. Department of Neuroscience, Medical University of South Carolina, Charleston, SC 29425, United States |
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| Abstract: | Brief epochs of pairing of low frequency synaptic activation and postsynaptic depolarization, in vitro, in supragranular neurons of mature guinea-pig visual cortex lead to a transient (20–60 min) synaptic potentiation. This process is due to a true up-regulation of excitatory synapse efficiency onto the activated neuron. The potentiation requires NMDA receptor activation and a postsynaptic calcium signal for induction and it is modifiable by endogenous nitric oxide (NO) production in the mature cortex. In the cortex of young animals (< PND 21), the pairing-induced potentiation is robust and depends on a postsynaptic calcium signal but it is independent of NMDA receptor activation and NO production. The ability of cortical synaptosomes to release endogenous glutamate is enhanced by NMDA receptor activation and this enhancement is NO-dependent. The NO signal, however, does not amplify the glutamate release of all synapses but only those that have activated voltage-gated calcium channels and were presumably more active at the time of the NO signal. Electrophysiological recordings from visual cortical neurons in anesthetized cats with local iontophoresis of compounds that inhibit or facilitate endogenous cortical NO production reveal the capacity for NO to modulate visual responses in vivo. NO appears to act in the intact cortex by amplifying signals of visual inputs that were co-active at the time of the NO production. The adult visual cortex is capable of dramatic alterations in synaptic efficiency over brief periods suggesting a dynamic cortical network. NMDA receptors and nitric oxide contribute to these processes. |
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