CiteULike: starz1010101's dendrites

Possible role of dendritic compartmentalization in the spatial working memory circuit.

K Morita — 2008-08-19T12:46:06-00:00

The Journal of neuroscience : the official journal of the Society for Neuroscience, Vol. 28, No. 30. (23 July 2008), pp. 7699-7724.

In spatial working memory tasks, pyramidal cells in the relevant cortical circuit receive massive inputs to shape stimulus location-selective sustained activity. A significant part of those inputs are applied onto the dendrites. Considering the dendritic morphology and circuit anatomy together with recently suggested branch-specific plasticity rules, external inputs transmitting the information of the stimulus location would be mapped onto some portion of the dendritic branches, rather than uniformly distributed over the branches. Meanwhile, recent studies revealed that each dendritic branch of pyramidal cell functions as a compartmentalized integration subunit through local spike generation and branch-specific excitation-inhibition interaction. I have examined how such nonlinear dendritic integration, combined with the nonuniform distribution of the external input, affects the behavior of the whole circuit by constructing a rate-coding model incorporating multiple dendritic branches of the individual pyramidal cell. Simulations varying the nature of dendritic nonlinearity and the configuration of somatically and dendritically mediated recurrent inhibition revealed that dendritic compartmentalization potentially enables the circuit to form an accurate memory depending on the contrast of the external input, but insensitively to its intensity, under certain conditions; in particular, when there exists tuned global dendritic recurrent inhibition or local dendritic inhibition coupled with global somatic inhibition. The model suggests that, when the circuit receives low-contrast or background input, only a small portion of dendritic branches of each pyramidal cell can overcome the local threshold so as to contribute to the somatic low-frequency firing, which in turn stabilizes the low-activity state of the circuit by recruiting recurrent inhibition.

Dendritic Backpropagation and the State of the Awake Neocortex

Yulia Bereshpolova — 2007-08-29T23:51:56-00:00

J. Neurosci., Vol. 27, No. 35. (29 August 2007), pp. 9392-9399.

The spread of somatic spikes into dendritic trees has become central to models of dendritic integrative properties and synaptic plasticity. However, backpropagating action potentials (BPAPs) have been studied mainly in slices, in which they are highly sensitive to multiple factors such as firing frequency and membrane conductance, raising doubts about their effectiveness in the awake behaving brain. Here, we examine the spatiotemporal characteristics of BPAPs in layer 5 pyramidal neurons in the visual cortex of adult, awake rabbits, in which EEG-defined brain states ranged from alert vigilance to drowsy/inattention, and, in some cases, to light sleep. To achieve this, we recorded extracellular spikes from layer 5 pyramidal neurons and field potentials above and below these neurons using a 16-channel linear probe, and applied methods of spike-triggered current source-density analysis to these records (Buzsaki and Kandel, 1998; Swadlow et al., 2002). Precise retinotopic alignment of superficial and deep cortical sites was used to optimize alignment of the recording probe with the axis of the apical dendrite. During the above network states, we studied BPAPs generated spontaneously, antidromically (from corticotectal neurons), or via intense synaptic drive caused by natural visual stimulation. Surprisingly, the invasion of BPAPs as far as 800 microm from the soma was little affected by the network state and only mildly attenuated by high firing frequencies. These data reveal that the BPAP is a robust and highly reliable property of neocortical apical dendrites. These events, therefore, are well suited to provide crucial signals for the control of synaptic plasticity during information-processing brain states. 10.1523/JNEUROSCI.2218-07.2007

Differential Cholinergic Modulation of Ca2+ Transients Evoked by Backpropagating Action Potentials in Apical and Basal Dendrites of Cortical Pyramidal Neurons

Kwang-Hyun Cho — 2008-06-25T15:42:45-00:00

J Neurophysiol, Vol. 99, No. 6. (1 June 2008), pp. 2833-2843.

The effect of the cholinergic agonist carbachol (CCh) on backpropagating action potential (bAP)-evoked Ca2+ transients in distal apical and basal dendrites of layer 2/3 pyramidal neurons in the primary visual cortex of rats was studied using whole cell recordings and confocal Ca2+ imaging. In the presence of CCh (20 microM), initial bAP-evoked Ca2+ transients were followed by large propagating secondary Ca2+ transients that were restricted to proximal apical dendrites [≤]40 microm from the soma. In middle apical dendrites (41-100 microm from the soma), Ca2+ transients evoked by AP bursts at 20 Hz, but not by single APs, were increased by CCh without secondary transients. CCh failed to increase the bAP-evoked Ca2+ transients in distal apical dendrites (101-270 microm from the soma). In contrast, in basal dendrites, CCh increased Ca2+ transients evoked by AP bursts, but not by single APs, and these transients were relatively constant over the entire length of the dendrites. CCh further increased the enhanced bAP-evoked Ca2+ transients in the presence of 4-aminopyridine (200 microM), an A-type K+ channel blocker, in basal and apical dendrites, except in distal apical dendrites. CCh increased large Ca2+ transients evoked by high-frequency AP bursts in basal dendrites, but not in distal apical dendrites. CCh-induced increase in Ca2+ transients was mediated by InsP3-dependent Ca2+-induced Ca2+-release. These results suggest that cholinergic stimulation differentially increases the bAP-evoked increase in [Ca2+]i in apical and basal dendrites, which may modulate synaptic activities in a location-dependent manner. 10.1152/jn.00063.2008

Backpropagation of physiological spike trains in neocortical pyramidal neurons: implications for temporal coding in dendrites.

SR Williams — 2007-03-07T15:55:57-00:00

J Neurosci, Vol. 20, No. 22. (15 November 2000), pp. 8238-8246.

In vivo neocortical neurons fire apparently random trains of action potentials in response to sensory stimuli. Does this randomness represent a signal or noise around a mean firing rate? Here we use the timing of action potential trains recorded in vivo to explore the dendritic consequences of physiological patterns of action potential firing in neocortical pyramidal neurons in vitro. We find that action potentials evoked by physiological patterns of firing backpropagate threefold to fourfold more effectively into the distal apical dendrites (>600 microm from the soma) than action potential trains reflecting their mean firing rate. This amplification of backpropagation was maximal during high-frequency components of physiological spike trains (80-300 Hz). The disparity between backpropagation during physiological and mean firing patterns was dramatically reduced by dendritic hyperpolarization. Consistent with this voltage dependence, dendritic depolarization amplified single action potentials by fourfold to sevenfold, with a spatial profile strikingly similar to the amplification of physiological spike trains. Local blockade of distal dendritic sodium channels substantially reduced amplification of physiological spike trains, but did not significantly alter action potential trains reflecting their mean firing rate. Dendritic electrogenesis during physiological spike trains was also reduced by the blockade of calcium channels. We conclude that amplification of backpropagating action potentials during physiological spike trains is mediated by frequency-dependent supralinear temporal summation, generated by the recruitment of distal dendritic sodium and calcium channels. Together these data indicate that the temporal nature of physiological patterns of action potential firing contains a signal that is transmitted effectively throughout the dendritic tree.

Active propagation of somatic action potentials into neocortical pyramidal cell dendrites.

GJ Stuart — 2005-08-18T23:27:39-00:00

Nature, Vol. 367, No. 6458. (6 January 1994), pp. 69-72.

The dendrites of neurons in the mammalian central nervous system have been considered as electrically passive structures which funnel synaptic potentials to the soma and axon initial segment, the site of action potential initiation. More recent studies, however, have shown that the dendrites of many neurons are not passive, but contain active conductances. The role of these dendritic voltage-activated channels in the initiation of action potentials in neurons is largely unknown. To assess this directly, patch-clamp recordings were made from the dendrites of neocortical pyramidal cells in brain slices. Voltage-activated sodium currents were observed in dendritic outside-out patches, while action potentials could be evoked by depolarizing current pulses or by synaptic stimulation during dendritic whole-cell recordings. To determine the site of initiation of these action potentials, simultaneous whole-cell recordings were made from the soma and the apical dendrite or axon of the same cell. These experiments showed that action potentials are initiated first in the axon and then actively propagate back into the dendritic tree.

Active dendrites: colorful wings of the mysterious butterflies.

Daniel Johnston — 2008-06-03T19:24:03-00:00

Trends in neurosciences (7 May 2008)

Santiago Ramón y Cajal had referred to neurons as the 'mysterious butterflies of the soul.' Wings of these butterflies - their dendrites - were traditionally considered as passive integrators of synaptic information. Owing to a growing body of experimental evidence, it is now widely accepted that these wings are colorful, endowed with a plethora of active conductances, with each family of these butterflies made of distinct hues and shades. Furthermore, rapidly evolving recent literature also provides direct and indirect demonstrations for activity-dependent plasticity of these active conductances, pointing toward chameleonic adaptability in these hues. These experimental findings firmly establish the immense computational power of a single neuron, and thus constitute a turning point toward the understanding of various aspects of neuronal information processing. In this brief historical perspective, we track important milestones in the chameleonic transmogrification of these mysterious butterflies.

Calcium electrogenesis in distal apical dendrites of layer 5 pyramidal cells at a critical frequency of back-propagating action potentials.

ME Larkum — 2008-06-02T18:30:05-00:00

Proceedings of the National Academy of Sciences of the United States of America, Vol. 96, No. 25. (7 December 1999), pp. 14600-14604.

Action potentials in juvenile and adult rat layer-5 neocortical pyramidal neurons can be initiated at both axonal and distal sites of the apical dendrite. However, little is known about the interaction between these two initiation sites. Here, we report that layer 5 pyramidal neurons are very sensitive to a critical frequency of back-propagating action potentials varying between 60 and 200 Hz in different neurons. Bursts of four to five back-propagating action potentials above the critical frequency elicited large regenerative potentials in the distal dendritic initiation zone. The critical frequency had a very narrow range (10-20 Hz), and the dendritic regenerative activity led to further depolarization at the soma. The dendritic frequency sensitivity was suppressed by blockers of voltage-gated calcium channels, and also by synaptically mediated inhibition. Calcium-fluorescence imaging revealed that the site of largest transient increase in intracellular calcium above the critical frequency was located 400-700 micrometer from the soma at the site for initiation of calcium action potentials. Thus, the distal dendritic initiation zone can interact with the axonal initiation zone, even when inputs to the neuron are restricted to regions close to the soma, if the output of the neuron exceeds a critical frequency.

The Back and Forth of Dendritic Plasticity

Stephen Williams — 2008-01-21T04:12:11-00:00

Neuron, Vol. 56, No. 6. (20 December 2007), pp. 947-953.

Synapses are located throughout the often-elaborate dendritic tree of central neurons. Hebbian models of plasticity require temporal association between synaptic input and neuronal output to produce long-term potentiation of excitatory transmission. Recent studies have highlighted how active dendritic spiking mechanisms control this association. Here, we review new work showing that associative synaptic plasticity can be generated without neuronal output and that the interplay between neuronal architecture and the active electrical properties of the dendritic tree regulates synaptic plasticity.

Hyperpolarization-activated current Ih disconnects somatic and dendritic spike initiation zones in layer V pyramidal neurons.

T Berger — 2008-05-13T18:15:45-00:00

Journal of neurophysiology, Vol. 90, No. 4. (October 2003), pp. 2428-2437.

Layer V pyramidal cells of the somatosensory cortex operate with two spike initiation zones. Subthreshold depolarizations are strongly attenuated along the apical dendrite linking the somatic and distal dendritic spike initiation zones. Sodium action potentials, on the other hand, are actively back-propagating from the axon hillock into the apical tuft. There they can interact with local excitatory input leading to the generation of calcium action potentials. We investigated if and how back-propagating sodium action potentials alone, without concomitant excitatory dendritic input, can initiate calcium action potentials in the distal dendrite. In acute slices of the rat somatosensory cortex, layer V pyramidal cells were studied under current-clamp with simultaneous recordings from the soma and the apical dendrite. A train of four somatic action potentials had to reach high frequencies to induce calcium action potentials in the dendrite ("critical frequency," CF approximately 100 Hz). Depolarization in the dendrite reduced the CF, while hyperpolarization increased it. The CF depended on the presence of the hyperpolarization-activated current Ih: blockade with 20 microM 4-(N-ethyl-N-phenylamino)-1,2-dimethyl-6-(methylamino) pyridinium chloride (ZD7288) reduced the CF to 68% of control. If the neurons were stimulated with noisy current injections, leading to in-vivo-like irregular spiking, no calcium action potentials were induced in the dendrite. However, after Ih channel blockade, calcium action potentials were frequently seen. These data suggest that Ih prevents initiation of the dendritic calcium action potential by proximal input alone. Dendritic calcium action potentials may therefore represent a unique signature for coincident somatic and dendritic activation.

alpha2-Adrenergic Receptors Modify Dendritic Spike Generation Via HCN Channels in the Prefrontal Cortex

Albert Barth — 2008-02-12T10:24:02-00:00

J Neurophysiol, Vol. 99, No. 1. (1 January 2008), pp. 394-401.

Although dendritic spikes are generally thought to be restricted to the distal apical dendrite, we know very little about the possible modulatory mechanisms that set the spatial limits of dendritic spikes. Our experiments demonstrated that high-frequency trains of backpropagating action potentials avoided filtering in the apical dendrite and initiated all-or-none dendritic Ca2+ transients associated with dendritic spikes in layer 5 pyramidal neurons of the prefrontal cortex. The block of hyperpolarization-activated currents (Ih) by ZD7288 could shift the frequency threshold and decreased the number of action potentials required to produce the all-or-none Ca2+ transient. Activation of alpha2-adrenergic receptors could also shift the frequency domain of spike induction to lower frequencies. Our data suggest that noradrenergic activity in the prefrontal cortex influences dendritic Ih and extends the zone of dendritic spikes in the apical dendrite via alpha2-adrenergic receptors. This mechanism might be one cellular correlate of the alpha2-receptormediated actions on working memory. 10.1152/jn.00943.2007

New angles on neuronal dendrites in vivo.

W Göbel — 2008-03-05T02:36:55-00:00

J Neurophysiol, Vol. 98, No. 6. (December 2007), pp. 3770-3779.

Imaging technologies are well suited to study neuronal dendrites, which are key elements for synaptic integration in the CNS. Dendrites are, however, frequently oriented perpendicular to tissue surfaces, impeding in vivo imaging approaches. Here we introduce novel laser-scanning modes for two-photon microscopy that enable in vivo imaging of spatiotemporal activity patterns in dendrites. First, we developed a method to image planes arbitrarily oriented in 3D, which proved particularly beneficial for calcium imaging of parallel fibers and Purkinje cell dendrites in rat cerebellar cortex. Second, we applied free linescans -- either through multiple dendrites or along a single vertically oriented dendrite -- to reveal fast dendritic calcium dynamics in neocortical pyramidal neurons. Finally, we invented a ribbon-type 3D scanning method for imaging user-defined convoluted planes enabling simultaneous measurements of calcium signals along multiple apical dendrites. These novel scanning modes will facilitate optical probing of dendritic function in vivo.

Supralinear Ca2+ influx into dendritic tufts of layer 2/3 neocortical pyramidal neurons in vitro and in vivo.

J Waters — 2008-03-05T02:16:21-00:00

J Neurosci, Vol. 23, No. 24. (17 September 2003), pp. 8558-8567.

Pyramidal neurons in layer 2/3 of the neocortex are central to cortical circuitry, but the intrinsic properties of their dendrites are poorly understood. Here we study layer 2/3 apical dendrites in parallel experiments in acute brain slices and in anesthetized rats using whole-cell recordings and Ca2+ imaging. We find that backpropagation of action potentials into the dendritic arbor is actively supported by Na+ channels both in vitro and in vivo. Single action potentials evoke substantial Ca2+ influx in the apical trunk but little or none in the dendritic tuft. Supralinear Ca2+ influx is produced in the tuft, however, when an action potential is paired with synaptic input. This dendritic supralinearity enables layer 2/3 neurons to integrate ascending sensory input from layer 4 and associative input to layer 1.

Spread of dendritic excitation in layer 2/3 pyramidal neurons in rat barrel cortex in vivo.

K Svoboda — 2008-03-04T21:24:05-00:00

Nat Neurosci, Vol. 2, No. 1. (January 1999), pp. 65-73.

In layer 2/3 pyramidal neurons of barrel cortex in vivo, calcium ion concentration ([Ca2+]) transients in apical dendrites evoked by sodium action potentials are limited to regions close to the soma. To study the mechanisms underlying this restricted pattern of calcium influx, we combined two-photon imaging of dendritic [Ca2+] dynamics with dendritic membrane potential measurements. We found that sodium action potentials attenuated and broadened rapidly with distance from the soma. However, dendrites of layer 2/3 cells were electrically excitable, and direct current injections could evoke large [Ca2+] transients. The restricted pattern of dendritic [Ca2+] transients is therefore due to a failure of sodium action-potential propagation into dendrites. Also, stimulating subcortical activating systems by tail pinch can enhance dendritic [Ca2+] influx induced by a sensory stimulus by increasing cellular excitability, consistent with the importance of these systems in plasticity and learning.

Integrative Properties of Radial Oblique Dendrites in Hippocampal CA1 Pyramidal Neurons.

A Losonczy — 2006-05-07T06:19:08-00:00

Neuron, Vol. 50, No. 2. (20 April 2006), pp. 291-307.

Although radial oblique dendrites are a major synaptic input site in CA1 pyramidal neurons, little is known about their integrative properties. We have used multisite two-photon glutamate uncaging to deliver different spatiotemporal input patterns to single branches while simultaneously recording the uncaging-evoked excitatory postsynaptic potentials and local Ca(2+) signals. Asynchronous input patterns sum linearly in spite of the spatial clustering and produce Ca(2+) signals that are mediated by NMDA receptors (NMDARs). Appropriately timed and sized input patterns ( approximately 20 inputs within approximately 6 ms) produce a supralinear summation due to the initiation of a dendritic spike. The Ca(2+) signals associated with synchronous input were larger and mediated by influx through both NMDARs and voltage-gated Ca(2+) channels (VGCCs). The oblique spike is a fast Na(+) spike whose duration is shaped by the coincident activation of NMDAR, VGCCs, and transient K(+) currents. Our results suggest that individual branches can function as single integrative compartments.