Locally distributed synaptic potentiation in the hippocampus.

The long-lasting increase in synaptic strength known as long-term potentiation has been advanced as a potential physiological mechanism for many forms of both developmental and adult neuronal plasticity. In many models of plasticity, intercellular communication has been proposed to account for observations in which simultaneously active neurons are strengthened together. The data presented here indicate that long-term potentiation can be communicated between synapses on neighboring neurons by means of a diffusible messenger. This distributed potentiation provides a mechanism for the cooperative strengthening of proximal synapses and may underlie a variety of plastic processes in the nervous system.

[1]  G. Lynch,et al.  Heterosynaptic depression: a postsynaptic correlate of long-term potentiation , 1977, Nature.

[2]  P. Andersen,et al.  Specific long-lasting potentiation of synaptic transmission in hippocampal slices , 1977, Nature.

[3]  G. Lynch,et al.  Intracellular injections of EGTA block induction of hippocampal long-term potentiation , 1983, Nature.

[4]  S. Kelso,et al.  Hebbian synapses in hippocampus. , 1986, Proceedings of the National Academy of Sciences of the United States of America.

[5]  R. Malinow,et al.  Postsynaptic hyperpolarization during conditioning reversibly blocks induction of long-term potentiation , 1986, Nature.

[6]  R S Zucker,et al.  Postsynaptic calcium is sufficient for potentiation of hippocampal synaptic transmission. , 1988, Science.

[7]  R. Nicoll,et al.  Tonic activation of NMDA receptors by ambient glutamate enhances excitability of neurons. , 1989, Science.

[8]  T. Bliss,et al.  Arachidonic acid induces a long-term activity-dependent enhancement of synaptic transmission in the hippocampus , 1989, Nature.

[9]  A. Aertsen,et al.  Synaptic plasticity in rat hippocampal slice cultures: local "Hebbian" conjunction of pre- and postsynaptic stimulation leads to distributed synaptic enhancement. , 1989, Proceedings of the National Academy of Sciences of the United States of America.

[10]  G. Edelman,et al.  The NO hypothesis: possible effects of a short-lived, rapidly diffusible signal in the development and function of the nervous system. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[11]  J. Bolz,et al.  Non-Hebbian synapses in rat visual cortex. , 1990, Neuroreport.

[12]  D. Prince,et al.  Double-labelling with rhodamine beads and biocytin: a technique for studying corticospinal and other projection neurons in vitro , 1991, Journal of Neuroscience Methods.

[13]  G. Edelman,et al.  Spatial signaling in the development and function of neural connections. , 1991, Cerebral cortex.

[14]  G. Böhme,et al.  Possible involvement of nitric oxide in long-term potentiation. , 1991, European journal of pharmacology.

[15]  E. Kandel,et al.  Tests of the roles of two diffusible substances in long-term potentiation: evidence for nitric oxide as a possible early retrograde messenger. , 1991, Proceedings of the National Academy of Sciences of the United States of America.

[16]  D. Madison,et al.  A requirement for the intercellular messenger nitric oxide in long-term potentiation. , 1991, Science.

[17]  D. Attwell,et al.  Potentiation of NMDA receptor currents by arachidonic acid , 1992, Nature.

[18]  E. Kandel,et al.  Are adult learning mechanisms also used for development? , 1992, Science.

[19]  M. Miras-Portugal,et al.  Positive feedback of glutamate exocytosis by metabotropic presynaptic receptor stimulation , 1992, Nature.

[20]  G. Lynch,et al.  Antagonists of the Platelet‐activating Factor Receptor Block Long‐term Potentiation in Hippocampal Slices , 1992, The European journal of neuroscience.

[21]  C. Zorumski,et al.  Enhancement of hippocampal excitatory synaptic transmission by platelet-activating factor , 1992, Neuron.

[22]  B. Ballyk,et al.  Elevation of extracellular potassium facilitates the induction of hippocampal long‐term potentiation , 1992, Journal of Neuroscience Research.

[23]  G. Collingridge,et al.  The Sharpey‐Schafer Prize Lecture. The mechanism of induction of NMDA receptor‐dependent long‐term potentiation in the hippocampus , 1992, Experimental physiology.

[24]  D. Clifford,et al.  Inhibition of long-term potentiation by NMDA-mediated nitric oxide release. , 1992, Science.

[25]  V. Gribkoff,et al.  Evidence for nitric oxide synthase inhibitor-sensitive and insensitive hippocampal synaptic potentiation. , 1992, Journal of neurophysiology.

[26]  George L. Wilcox,et al.  The role of nitric oxide in hippocampal long-term potentiation , 1992, Neuron.

[27]  M. V. Hogan,et al.  Long-term potentiation in the hippocampus induced by platelet-activating factor , 1993, Neuron.

[28]  Charles F. Stevens,et al.  Reversal of long-term potentiation by inhibitors of haem oxygenase , 1993, Nature.

[29]  K. Murphy,et al.  The suppression of long-term potentiation in rat hippocampus by inhibitors of nitric oxide synthase is temperature and age dependent , 1993, Neuron.

[30]  E. Kandel,et al.  Nitric oxide and carbon monoxide produce activity-dependent long-term synaptic enhancement in hippocampus. , 1993, Science.

[31]  P. Chapman,et al.  Nitric oxide synthase inhibitors block long-term potentiation induced by weak but not strong tetanic stimulation at physiological brain temperatures in rat hippocampal slices , 1993, Neuroscience Letters.

[32]  J. Sweatt,et al.  Nitric oxide synthase-independent long-term potentiation in area CA1 of hippocampus. , 1993, Neuroreport.