All-or-none potentiation at CA3-CA1 synapses.

The molecular mechanisms underlying long-term potentiation in the hippocampus have received much attention because of the likely functional importance of synaptic plasticity for information storage and the development of neuronal connectivity. Surprisingly, it remains unclear whether activity modifies the strength of individual synapses in a digital (all-or-none) or analog (graded) manner. Here we characterize step-like all-or-none transitions from baseline synaptic transmission to potentiated states following protocols for inducing potentiation at putative single CA3-CA1 synaptic connections. Individual synapses appear to have all-or-none potentiation indicative of highly cooperative processes but different thresholds for undergoing potentiation. These results raise the possibility that some forms of synaptic memory may be stored in a digital manner in the brain.

[1]  J. Lisman A mechanism for memory storage insensitive to molecular turnover: a bistable autophosphorylating kinase. , 1985, Proceedings of the National Academy of Sciences of the United States of America.

[2]  Allen I. Selverston,et al.  Model Neural Networks and Behavior , 1985, Springer US.

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

[4]  D. Tank,et al.  Optical imaging of calcium accumulation in hippocampal pyramidal cells during synaptic activation , 1989, Nature.

[5]  H. Wigström,et al.  Onset Characteristics of Long‐Term Potentiation in the Guinea‐Pig Hippocampal CA1 Region in Vitro , 1989, The European journal of neuroscience.

[6]  Arnold R. Kriegstein,et al.  Whole cell recording from neurons in slices of reptilian and mammalian cerebral cortex , 1989, Journal of Neuroscience Methods.

[7]  R. Malenka,et al.  Characterization of the integration time for the stabilization of long- term potentiation in area CA1 of the hippocampus , 1992, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[8]  Alcino J. Silva,et al.  Deficient hippocampal long-term potentiation in alpha-calcium-calmodulin kinase II mutant mice. , 1992, Science.

[9]  R. Malenka,et al.  Temporal limits on the rise in postsynaptic calcium required for the induction of long-term potentiation , 1992, Neuron.

[10]  R. Malenka,et al.  Mechanisms underlying induction of homosynaptic long-term depression in area CA1 of the hippocampus , 1992, Neuron.

[11]  T. Bliss,et al.  A synaptic model of memory: long-term potentiation in the hippocampus , 1993, Nature.

[12]  R. Nicoll,et al.  NMDA-receptor-dependent synaptic plasticity: multiple forms and mechanisms , 1993, Trends in Neurosciences.

[13]  C. Stevens,et al.  Changes in reliability of synaptic function as a mechanism for plasticity , 1994, Nature.

[14]  Lubert Stryer,et al.  Dual role of calmodulin in autophosphorylation of multifunctional cam kinase may underlie decoding of calcium signals , 1994, Neuron.

[15]  R. Malinow,et al.  Potentiated transmission and prevention of further LTP by increased CaMKII activity in postsynaptic hippocampal slice neurons. , 1994, Science.

[16]  J. Isaac,et al.  Evidence for silent synapses: Implications for the expression of LTP , 1995, Neuron.

[17]  R. Malinow,et al.  Activation of postsynaptically silent synapses during pairing-induced LTP in CA1 region of hippocampal slice , 1995, Nature.

[18]  R. Nicoll,et al.  Contrasting properties of two forms of long-term potentiation in the hippocampus , 1995, Nature.

[19]  Dimitri M. Kullmann,et al.  The site of expression of NMDA receptor-dependent LTP: New fuel for an old fire , 1995, Neuron.

[20]  J. Jack,et al.  Synaptic plasticity: hippocampal LTP , 1995, Current Opinion in Neurobiology.

[21]  S. Siegelbaum,et al.  Regulation of hippocampal transmitter release during development and long-term potentiation. , 1995, Science.

[22]  R. Nicoll,et al.  Calcium/calmodulin-dependent kinase II and long-term potentiation enhance synaptic transmission by the same mechanism. , 1995, Proceedings of the National Academy of Sciences of the United States of America.

[23]  Robert S. Zucker,et al.  Postsynaptic Levels of [Ca2+]i Needed to Trigger LTD and LTP , 1996, Neuron.

[24]  A. Konnerth,et al.  Long-term potentiation and functional synapse induction in developing hippocampus , 1996, Nature.

[25]  M. Bear,et al.  Metaplasticity: the plasticity of synaptic plasticity , 1996, Trends in Neurosciences.

[26]  T. Soderling,et al.  Regulatory phosphorylation of AMPA-type glutamate receptors by CaM-KII during long-term potentiation. , 1997, Science.

[27]  Alcino J. Silva,et al.  Autophosphorylation at Thr286 of the alpha calcium-calmodulin kinase II in LTP and learning. , 1998, Science.

[28]  R. Nicoll,et al.  Postsynaptic membrane fusion and long-term potentiation. , 1998, Science.