Compartmentalized and Binary Behavior of Terminal Dendrites in Hippocampal Pyramidal Neurons

Wei, Dongsheng; Mei, Yan‐Ai; Bagal, Ashish A.; Kao, Joseph P. Y.; Thompson, Scott M.; Tang, Cha‐Min

doi:10.1126/science.1061198

Cited by 186 publications

(209 citation statements)

References 16 publications

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“…The tuft spikes that we observe in AOB mitral cells also have many properties in common with NMDA spikes (Schiller et al, 2000;Polsky et al, 2004) and other isolated dendritic events seen in pyramidal cells (Golding and Spruston, 1998;Wei et al, 2001). Tuft spikes in AOB mitral cells seem to depend critically on NMDAR activation, like similar phenomena observed in cortical pyramidal cells (Schiller et al, 2000;Wei et al, 2001).…”

Section: Comparison To Other Dendritesmentioning

confidence: 56%

“…Because locally isolated calcium events in dendrites of other cell types seem to depend on NMDA receptor activation (Wei et al, 2001;Polsky et al, 2004), we tested to see whether these events were blocked by application of the NMDA receptor blocker APV (50 M). Addition of APV resulted in substantial, but incomplete, reduction in the amplitude of isolated calcium transients in the mitral cell tufts (23 Ϯ 16% of control; n ϭ 6; p Ͻ 0.05) (Fig.…”

Section: Synaptically Evoked Calcium Transientsmentioning

confidence: 99%

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Tuft Calcium Spikes in Accessory Olfactory Bulb Mitral Cells

Urban

Castro²

2005

J. Neurosci.

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The mammalian accessory olfactory system is critical for the detection and identification of pheromones and the representation of complex stimuli including sex, genetic relatedness, and individual identity. Mitral cells, the principal cells of the accessory olfactory bulb (AOB), receive monosynaptic input from the sensory periphery and already show highly specific response properties, firing selectively for combinations of genetic markers and gender-specific cues. Vomeronasal sensory neuron axons form synapses onto distal tuft-like branches of mitral cell primary dendrites. We have studied dendritic excitability and synaptic integration in AOB mitral cell dendrites, and we show that dendrites of accessory olfactory bulb mitral cells support action potential propagation and can fire regenerative spike-like events that are likely to contribute to the integration of inputs to these cells. These tuft spikes may be important for the specificity of AOB mitral cell responses.

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Section: Comparison To Other Dendritesmentioning

confidence: 56%

Section: Synaptically Evoked Calcium Transientsmentioning

confidence: 99%

Tuft Calcium Spikes in Accessory Olfactory Bulb Mitral Cells

Urban

Castro²

2005

J. Neurosci.

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“…Recently, Ariav et al, (2003) used calcium imaging to determine the origin of fast spikes in CA1 hippocampal neurons. It is well known that the slow component of the synapticallyevoked or glutamate-evoked transient causes strong calcium elevations in thin dendritic branches of neocortical (Schiller et al, 2000) and hippocampal pyramidal neurons (Regehr & Tank, 1990;Wei et al, 2001). Calcium ions stream into the dendritic cytosol through either NMDA receptor channels (Schiller et al, 2000), voltage-gated calcium channels (VGCC) (Oakley, Schwindt & Crill, 2001a;Wei et al, 2001), or both, NMDA and VGCC channels.…”

Section: Discussionmentioning

confidence: 99%

“…It is well known that the slow component of the synapticallyevoked or glutamate-evoked transient causes strong calcium elevations in thin dendritic branches of neocortical (Schiller et al, 2000) and hippocampal pyramidal neurons (Regehr & Tank, 1990;Wei et al, 2001). Calcium ions stream into the dendritic cytosol through either NMDA receptor channels (Schiller et al, 2000), voltage-gated calcium channels (VGCC) (Oakley, Schwindt & Crill, 2001a;Wei et al, 2001), or both, NMDA and VGCC channels. Because fast spikes were always accompanied by a slow component, the calcium imaging data by Ariav et al, (2003) cannot be used to determine the site of origin, or to describe any other characteristics of fast spikes in the dendrites.…”

Section: Discussionmentioning

confidence: 99%

Initiation of Sodium Spikelets in Basal Dendrites of Neocortical Pyramidal Neurons

et al. 2005

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Cortical information processing relies critically on the processing of electrical signals in pyramidal neurons. Electrical transients mainly arise when excitatory synaptic inputs impinge upon distal dendritic regions. To study the dendritic aspect of synaptic integration one must record electrical signals in distal dendrites. Since thin dendritic branches, such as oblique and basal dendrites, do not support routine glass electrode measurements, we turned our effort towards voltage-sensitive dye recordings. Using the optical imaging approach we found and reported previously that basal dendrites of neocortical pyramidal neurons show an elaborate repertoire of electrical signals, including backpropagating action potentials and glutamate-evoked plateau potentials. Here we report a novel form of electrical signal, qualitatively and quantitatively different from backpropagating action potentials and dendritic plateau potentials. Strong glutamatergic stimulation of an individual basal dendrite is capable of triggering a fast spike, which precedes the dendritic plateau potential. The amplitude of the fast initial spikelet was actually smaller that the amplitude of the backpropagating action potential in the same dendritic segment. Therefore, the fast initial spike was dubbed "spikelet". Both the basal spikelet and plateau potential propagate decrementally towards the cell body, where they are reflected in the somatic whole-cell recordings. The low incidence of basal spikelets in the somatic intracellular recordings and the impact of basal spikelets on soma-axon action potential initiation are discussed.

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“…Note that Sjö strö m and colleagues were able to induce LTP with low frequency pairing when the soma was mildly depolarized. (34) Although the chemical consequences at the synapse remain unknown, it is tempting to imagine that this depolarization leads to calcium spikes in dendritic branchlets, (87,88) such that the frequency-dependence of CaM activation is dramatically altered by an additional mode of Ca 2þ entry. Future direction Clearly, this model does yet not explain the differences between the intracellular Ca 2þ dynamics required for the induction of LTP and LTD, or the critical time-window of STDP.…”

Section: Epsp-induced Ca 2þ Influxmentioning

confidence: 99%

Complexity of calcium signaling in synaptic spines

Franks¹,

Sejnowski²

2002

BioEssays

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SummaryLong-term potentiation and long-term depression are thought to be cellular mechanisms contributing to learning and memory. Although the physiological phenomena have been well characterized, little consensus of their underlying molecular mechanisms has emerged. One reason for this may be the under-appreciated complexity of the signaling pathways that can arise if key signaling molecules are discretely localized within the synapse. Recent findings suggest an unanticipated degree of structural organization at the synapse, and improved methods in cellular imaging of living tissue have provided much-needed information about the intracellular dynamics of Ca 2þ , thought to be critical for both LTP and LTD. In this review, we briefly summarize some of these developments, and show that a more complete understanding of cellular signaling depends on the successful integration of traditional biochemistry and molecular biology with the spatial and temporal details of synaptic ultrastructure. Biophysically realistic computer simulations can have an important role in bridging these disciplines.

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Compartmentalized and Binary Behavior of Terminal Dendrites in Hippocampal Pyramidal Neurons

Cited by 186 publications

References 16 publications

Tuft Calcium Spikes in Accessory Olfactory Bulb Mitral Cells

Tuft Calcium Spikes in Accessory Olfactory Bulb Mitral Cells

Initiation of Sodium Spikelets in Basal Dendrites of Neocortical Pyramidal Neurons

Complexity of calcium signaling in synaptic spines

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