Miniature neurotransmission stabilizes synaptic function via tonic suppression of local dendritic protein synthesis.

@article{citeulike:748941, abstract = {Activity deprivation in neurons induces a slow compensatory scaling up of synaptic strength, reflecting a homeostatic mechanism for stabilizing neuronal activity. Prior studies have focused on the loss of action potential (AP) driven neurotransmission in synaptic homeostasis. Here, we show that the miniature synaptic transmission that persists during AP blockade profoundly shapes the time course and mechanism of homeostatic scaling. A brief blockade of NMDA receptor (NMDAR) mediated miniature synaptic events ("minis") rapidly scales up synaptic strength, over an order of magnitude faster than with AP blockade alone. The rapid scaling induced by NMDAR mini blockade is mediated by increased synaptic expression of surface GluR1 and the transient incorporation of Ca2+-permeable AMPA receptors at synapses; both of these changes are implemented locally within dendrites and require dendritic protein synthesis. These results indicate that NMDAR signaling during miniature synaptic transmission serves to stabilize synaptic function through active suppression of dendritic protein synthesis.}, address = {Division of Biology 114-96, California Institute of Technology, Pasadena, CA 91125, USA.}, author = {Sutton, M. A. and Ito, H. T. and Cressy, P. and Kempf, C. and Woo, J. C. and Schuman, E. M. }, citeulike-article-id = {748941}, comment = {Journal Club du 20/09/06}, doi = {10.1016/j.cell.2006.03.040}, issn = {0092-8674}, journal = {Cell}, keywords = {dendrites, electrophysiology, journal\_club, local\_synthesis, membrane\_insertion, postsynaptic, synapse}, month = {May}, number = {4}, pages = {785--799}, posted-at = {2006-09-20 12:34:01}, priority = {0}, title = {Miniature neurotransmission stabilizes synaptic function via tonic suppression of local dendritic protein synthesis.}, url = {http://dx.doi.org/10.1016/j.cell.2006.03.040}, volume = {125}, year = {2006} }

TY - JOUR ID - citeulike:748941 L3 - citeulike-article-id:748941 TI - Miniature neurotransmission stabilizes synaptic function via tonic suppression of local dendritic protein synthesis. JF - Cell VL - 125 IS - 4 SP - 785 EP - 799 AD - Division of Biology 114-96, California Institute of Technology, Pasadena, CA 91125, USA. SN - 0092-8674 N2 - Activity deprivation in neurons induces a slow compensatory scaling up of synaptic strength, reflecting a homeostatic mechanism for stabilizing neuronal activity. Prior studies have focused on the loss of action potential (AP) driven neurotransmission in synaptic homeostasis. Here, we show that the miniature synaptic transmission that persists during AP blockade profoundly shapes the time course and mechanism of homeostatic scaling. A brief blockade of NMDA receptor (NMDAR) mediated miniature synaptic events ("minis") rapidly scales up synaptic strength, over an order of magnitude faster than with AP blockade alone. The rapid scaling induced by NMDAR mini blockade is mediated by increased synaptic expression of surface GluR1 and the transient incorporation of Ca2+-permeable AMPA receptors at synapses; both of these changes are implemented locally within dendrites and require dendritic protein synthesis. These results indicate that NMDAR signaling during miniature synaptic transmission serves to stabilize synaptic function through active suppression of dendritic protein synthesis. KW - dendrites KW - electrophysiology KW - journal_club KW - local_synthesis KW - membrane_insertion KW - postsynaptic KW - synapse N1 - Journal Club du 20/09/06 AU - Sutton, MA AU - Ito, HT AU - Cressy, P AU - Kempf, C AU - Woo, JC AU - Schuman, EM PY - 2006/05/19/ UR - http://dx.doi.org/10.1016/j.cell.2006.03.040 ER -