Dendritic spikes as a mechanism for cooperative long-term potentiation
By Nace L. Golding, Nathan P. Staff, Nelson Spruston. 2002
648 citations recorded by the source corpus.
Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Electrical and Electronic Engineering
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cellular and Molecular Neuroscience
- Wulfram Gerstner
- Friedemann Zenke
- György Buzsáki
- D. Feldman
- Loren M. Frank
- Robert Froemke
- Claudia Clopath
- Nicolas Frémaux
In Cognitive Neuroscience
- Wulfram Gerstner
- Friedemann Zenke
- György Buzsáki
- D. Feldman
- Loren M. Frank
- Claudia Clopath
- Xiao-Jing Wang
- Robert Froemke
In Electrical and Electronic Engineering
- Wulfram Gerstner
- Friedemann Zenke
- D. Feldman
- Claudia Clopath
- Pierre Yger
- Henry Markram
- Nicolas Frémaux
- Y. Dan
Citations in the corpus
- Network Oscillations: Emerging Computational Principles (2006, background): “Correlations in input activity can induce synaptic plasticity (Bliss and Lomo, 1973; McNaughton and Douglas, 1978; Golding et al., 2002); if the salient inputs were correlated, they would automatically increase the likelihood that this information would be stored in memory.”
- A History of Spike-Timing-Dependent Plasticity (2011, background): “Clearly, strong depolarization elicits more spikes and potentially stronger potentiation, but abolishing spikes does not necessarily prevent such strong depolarizationinduced plasticity (Golding et al., 2002; Remy and Spruston, 2007; Hardie and Spruston, 2009).”
- Integrative properties of radial oblique dendrites in hippocampal CA1 pyramidal neurons. (2006, background): “The large local Ca 2+ signals recorded here could be involved in producing several different forms of synaptic and nonsynaptic plasticity (Golding et al., 2002; Holthoff et al., 2004), that depending on the spatial pattern of the input could expand to encompass all of the synapses on the entire…”
- Neuromodulated Spike-Timing-Dependent Plasticity, and Theory of Three-Factor Learning Rules (2016, background): “Noradrenaline emission linked to arousal caused by novel stimuli could favor “the development of persistent facilitatory changes in all synapses that are currently in a state of excitation” as suggested by early conceptual theories (Kety, 1972); cited and evidence discussed in Sara (2009).”
- The spike timing dependence of plasticity (2012, background): “Very distal synapses may be largely outside the influence of bAPs, so that STDP is absent and plasticity is induced by cooperative firing of neighboring inputs that evokes dendritic sodium or calcium spikes or regenerative NMDA spikes (Golding et al., 2002; Gordon et al., 2006).”
- Hippocampal mechanisms for the context-dependent retrieval of episodes (2005, neutral): “modification due to presynaptic spiking interacting with dendritic spikes ( Golding, Staff, & Spruston, 2002 ).”
- Inhibition as a Binary Switch for Excitatory Plasticity in Pyramidal Neurons (2016, background): “Because calcium spikes can also serve as plasticity signals [26], we analyzed the effects of inhibition on bAPs and calcium spikes during this firing mode.”
- Requirement of dendritic calcium spikes for induction of spike‐timing‐dependent synaptic plasticity (2006, background): “…correlated synaptic inputs in the absence of APs (Schiller et al. 1997), with recent work in pyramidal neurons in the hippocampus indicating a role of dendritic calcium spikes in the induction of non-Hebbian forms of synaptic plasticity that do not require backpropagating APs (Golding et al. 2002).”
- Elements of a neurobiological theory of the hippocampus: the role of activity-dependent synaptic plasticity in memory. (2003, background): “Dark red indicates maximum rate (left to right: 8, 12, 12, 17 and 11 Hz). sufficient to trigger somatic actional potentials in these cells; reliable discharge may require summation of EPSPs, i.e. high afferent firing rates (Golding & Spruston 1998; Golding et al. 2002).”
- Pyramidal neurons: dendritic structure and synaptic integration (2008, background): “Furthermore, pairing action potentials with small EPSPs in the apical tuft of CA1 pyramidal neurons does not induce LTP, presumably because action potentials do not propagate reliably to this distal locatio”
- What is the function of hippocampal theta rhythm?—Linking behavioral data to phasic properties of field potential and unit recording data (2005, background): “LTP even when the soma is hyperpolarized (Golding et al., 2002).”
- The role of interneuron networks in driving human motor cortical plasticity. (2013, result): “Our results would therefore be compatible with the idea that the oligosynaptic inputs evoked on distal dendrites behave differently to the monosynaptic proximal inputs (Golding et al. 2002; Branco and Hausser 2011).”
- Reactivation of experience-dependent cell assembly patterns in the hippocampus (2008, background): “Another line of work has shown that dendritic depolarization is sufficient for plasticity in CA1 cells; back-propagating action potentials (needed for STDP) are not require”
- Single‐shock LTD by local dendritic spikes in pyramidal neurons of mouse visual cortex (2004, background): “A recent study (Golding et al. 2002) has demonstrated that, in conditions of suppressed synaptic inhibition, multiple dendritic spikes, produced by afferent theta burst stimulation, evoke long-term potentiation (LTP) in hippocampal pyramidal neurons.”
- Hippocampal Plasticity across Multiple Days of Exposure to Novel Environments (2004, positive): “, dendritic spikes) (Golding et al., 2002) or reorganizations of the entorhinal cortical and CA3 inputs to CA1 (Amaral and Witter, 1995).”