scholarly journals A Localized Scaffold for cGMP Increase Is Required for Apical Dendrite Development

Cell Reports ◽  
2020 ◽  
Vol 31 (2) ◽  
pp. 107519
Author(s):  
Joanna Szczurkowska ◽  
Seong-Il Lee ◽  
Alan Guo ◽  
Andrzej W. Cwetsch ◽  
Tanvir Khan ◽  
...  
Keyword(s):  
Apical Dendrite ◽  
Dendrite Development

Effect of Common Anesthetics on Dendritic Properties in Layer 5 Neocortical Pyramidal Neurons

2008 ◽  
Vol 99 (3) ◽  
pp. 1394-1407 ◽  
Author(s):  
Sarah Potez ◽  
Matthew E. Larkum
Keyword(s):  
High Frequency ◽  
Pyramidal Neurons ◽  
Animal Experiments ◽  
Apical Dendrite ◽  
Network Activity ◽  
Calcium Spikes ◽  
Firing Properties ◽  
The Impact

Understanding the impact of active dendritic properties on network activity in vivo has so far been restricted to studies in anesthetized animals. However, to date no study has been made to determine the direct effect of the anesthetics themselves on dendritic properties. Here, we investigated the effects of three types of anesthetics commonly used for animal experiments (urethane, pentobarbital and ketamine/xylazine). We investigated the generation of calcium spikes, the propagation of action potentials (APs) along the apical dendrite and the somatic firing properties in the presence of anesthetics in vitro using dual somatodendritic whole cell recordings. Calcium spikes were evoked with dendritic current injection and high-frequency trains of APs at the soma. Surprisingly, we found that the direct actions of anesthetics on calcium spikes were very different. Two anesthetics (urethane and pentobarbital) suppressed dendritic calcium spikes in vitro, whereas a mixture of ketamine and xylazine enhanced them. Propagation of spikes along the dendrite was not significantly affected by any of the anesthetics but there were various changes in somatic firing properties that were highly dependent on the anesthetic. Last, we examined the effects of anesthetics on calcium spike initiation and duration in vivo using high-frequency trains of APs generated at the cell body. We found the same anesthetic-dependent direct effects in addition to an overall reduction in dendritic excitability in anesthetized rats with all three anesthetics compared with the slice preparation.

Distance-Dependent Ni2+-Sensitivity of Synaptic Plasticity in Apical Dendrites of Hippocampal CA1 Pyramidal Cells

2002 ◽  
Vol 87 (2) ◽  
pp. 1169-1174 ◽  
Author(s):  
Yoshikazu Isomura ◽  
Yoko Fujiwara-Tsukamoto ◽  
Michiko Imanishi ◽  
Atsushi Nambu ◽  
Masahiko Takada
Keyword(s):  
Calcium Influx ◽  
Critical Role ◽  
Field Potential ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Apical Dendrite ◽  
Excitatory Postsynaptic Potential ◽  
Distal Dendrite ◽  
Ca1 Pyramidal Cells ◽  
Hippocampal Ca1

Low concentration of Ni2+, a T- and R-type voltage-dependent calcium channel (VDCC) blocker, is known to inhibit the induction of long-term potentiation (LTP) in the hippocampal CA1 pyramidal cells. These VDCCs are distributed more abundantly at the distal area of the apical dendrite than at the proximal dendritic area or soma. Therefore we investigated the relationship between the Ni2+-sensitivity of LTP induction and the synaptic location along the apical dendrite. Field potential recordings revealed that 25 μM Ni2+ hardly influenced LTP at the proximal dendritic area (50 μm distant from the somata). In contrast, the same concentration of Ni2+ inhibited the LTP induction mildly at the middle dendritic area (150 μm) and strongly at the distal dendritic area (250 μm). Ni2+ did not significantly affect either the synaptic transmission at the distal dendrite or the burst-firing ability at the soma. However, synaptically evoked population spikes recorded near the somata were slightly reduced by Ni2+ application, probably owing to occlusion of dendritic excitatory postsynaptic potential (EPSP) amplification. Even when the stimulating intensity was strengthened sufficiently to overcome such a reduction in spike generation during LTP induction, the magnitude of distal LTP was not significantly recovered from the Ni2+-dependent inhibition. These results suggest that Ni2+ may inhibit the induction of distal LTP directly by blocking calcium influx through T- and/or R-type VDCCs. The differentially distributed calcium channels may play a critical role in the induction of LTP at dendritic synapses of the hippocampal pyramidal cells.

scholarly journals Apical length governs computational diversity of L5 pyramidal neurons

2019 ◽  
Author(s):  
Alessandro R. Galloni ◽  
Aeron Laffere ◽  
Ede Rancz
Keyword(s):  
Action Potentials ◽  
Pyramidal Neurons ◽  
Apical Dendrite ◽  
Common Assumption ◽  
Dendritic Excitability ◽  
Visual Cortices ◽  
The Common ◽  
Channel Dependent ◽  
Apical Dendrites ◽  
The Brain

AbstractAnatomical similarity across the neocortex has led to the common assumption that the circuitry is modular and performs stereotyped computations. Layer 5 pyramidal neurons (L5PNs) in particular are thought to be central to cortical computation because of their extensive arborisation and nonlinear dendritic operations. Here, we demonstrate that computations associated with dendritic Ca2+ plateaus in L5PNs vary substantially between the primary and secondary visual cortices. L5PNs in the secondary visual cortex show reduced dendritic excitability and smaller propensity for burst firing. This reduced excitability is correlated with shorter apical dendrites. Using numerical modelling, we uncover a universal principle underlying the influence of apical length on dendritic backpropagation and excitability, based on a Na+ channel-dependent broadening of backpropagating action potentials. In summary, we provide new insights into the modulation of dendritic excitability by apical dendrite length and show that the operational repertoire of L5 neurons is not universal throughout the brain.

scholarly journals Dendrites with specialized glial attachments develop by retrograde extension using SAX-7 and GRDN-1

2019 ◽  
Author(s):  
Elizabeth R. Cebul ◽  
Ian G. McLachlan ◽  
Maxwell G. Heiman
Keyword(s):  
Glial Cell ◽  
Molecular Mechanism ◽  
Mammalian Brain ◽  
Cytoplasmic Protein ◽  
Genetic Screens ◽  
Sense Organs ◽  
Adhesion Protein ◽  
C Elegans ◽  
Dendrite Development ◽  
Forward Genetic Screens

ABSTRACTDendrites develop elaborate morphologies in concert with surrounding glia, but the molecules that coordinate dendrite and glial morphogenesis are mostly unknown.C. elegansoffers a powerful model for identifying such factors. Previous work in this system examined dendrites and glia that develop within epithelia, similar to mammalian sense organs. Here, we focus on the neurons BAG and URX, which are not part of an epithelium but instead form membranous attachments to a single glial cell at the nose, reminiscent of dendrite-glia contacts in the mammalian brain. We show that these dendrites develop by retrograde extension, in which the nascent dendrite endings anchor to the presumptive nose and then extend by stretch during embryo elongation. Using forward genetic screens, we find that dendrite development requires the adhesion protein SAX-7/L1CAM and the cytoplasmic protein GRDN-1/CCDC88C to anchor dendrite endings at the nose. SAX-7 acts in neurons and glia, while GRDN-1 acts in glia to non-autonomously promote dendrite extension. Thus, this work shows how glial factors can help to shape dendrites, and identifies a novel molecular mechanism for dendrite growth by retrograde extension.

scholarly journals Quantitative synapse analysis for cell-type specific connectomics

2018 ◽  
Author(s):  
Dika A. Kuljis ◽  
Khaled Zemoura ◽  
Cheryl A. Telmer ◽  
Jiseok Lee ◽  
Eunsol Park ◽  
...  
Keyword(s):  
Large Scale ◽  
Neural Circuit ◽  
Apical Dendrite ◽  
Automated Detection ◽  
Cell Type ◽  
Disease States ◽  
Specific Localization ◽  
Cell Type Specific ◽  
Dendritic Branches ◽  
Circuit Function

AbstractAnatomical methods for determining cell-type specific connectivity are essential to inspire and constrain our understanding of neural circuit function. We developed new genetically-encoded reagents for fluorescence-synapse labeling and connectivity analysis in brain tissue, using a fluorogen-activating protein (FAP)-or YFP-coupled, postsynaptically-localized neuroligin-1 targeting sequence (FAP/YFPpost). Sparse viral expression of FAP/YFPpost with the cell-filling, red fluorophore dTomato (dTom) enabled high-throughput, compartment-specific localization of synapses across diverse neuron types in mouse somatosensory cortex. High-resolution confocal image stacks of virally-transduced neurons were used for 3D reconstructions of postsynaptic cells and automated detection of synaptic puncta. We took advantage of the bright, far-red emission of FAPpost puncta for multichannel fluorescence alignment of dendrites, synapses, and presynaptic neurites to assess subtype-specific inhibitory connectivity onto L2 neocortical pyramidal (Pyr) neurons. Quantitative and compartment-specific comparisons show that PV inputs are the dominant source of inhibition at both the soma and across all dendritic branches examined and were particularly concentrated at the primary apical dendrite, a previously unrecognized compartment of L2 Pyr neurons. Our fluorescence-based synapse labeling reagents will facilitate large-scale and cell-type specific quantitation of changes in synaptic connectivity across development, learning, and disease states.

scholarly journals Wnt7b signalling through Frizzled-7 receptor promotes dendrite development by coactivating CaMKII and JNK

2018 ◽  
Vol 131 (13) ◽  
pp. jcs216101 ◽  
Author(s):  
María E. Ferrari ◽  
María E. Bernis ◽  
Faye McLeod ◽  
Marina Podpolny ◽  
Romina P. Coullery ◽  
...  
Keyword(s):  
Dendrite Development

Response Properties and Synchronization of Rhythmically Firing Dendritic Neurons

2007 ◽  
Vol 97 (1) ◽  
pp. 208-219 ◽  
Author(s):  
Joshua A. Goldberg ◽  
Chris A. Deister ◽  
Charles J. Wilson
Keyword(s):  
Pyramidal Neurons ◽  
Phase Response Curve ◽  
Qualitative Difference ◽  
Apical Dendrite ◽  
Neuronal Firing ◽  
Closed Form Expression ◽  
Pass Filter ◽  
Cortical Pyramidal Neurons ◽  
The Impact ◽  
High Pass

The responsiveness of rhythmically firing neurons to synaptic inputs is characterized by their phase-response curve (PRC), which relates how weak somatic perturbations affect the timing of the next action potential. The shape of the somatic PRC is an important determinant of collective network dynamics. Here we study theoretically and experimentally the impact of distally located synapses and dendritic nonlinearities on the synchronization properties of rhythmically firing neurons. By combining the theories of quasi-active cables and phase-coupled oscillators we derive an approximation for the dendritic responsiveness, captured by the neuron's dendritic PRC (dPRC). This closed-form expression indicates that the dPRCs are linearly filtered versions of the somatic PRC and that the filter characteristics are determined by the passive and active properties of the dendrite. The passive properties induce leftward shifts in the dPRCs and attenuate them. Our analysis yields a single dimensionless parameter that classifies active dendritic conductances as either regenerative conductances that counter the passive properties by boosting the dPRCs or restorative conductances that high-pass filter the dPRCs. Thus dendritic properties can generate a qualitative difference between the somatic and dendritic PRCs. As a result collective dynamics can be qualitatively different depending on the location of the synapse, the neuronal firing rates, and the dendritic nonlinearities. Finally, we use dual whole cell recordings from the soma and apical dendrite of cortical pyramidal neurons to test these predictions and find that empirical dPRCs are shifted leftward, as predicted, but may also display high-pass characteristics resulting from the restorative dendritic HCN (h) current.

scholarly journals Site Independence of EPSP Time Course Is Mediated by DendriticI h in Neocortical Pyramidal Neurons

2000 ◽  
Vol 83 (5) ◽  
pp. 3177-3182 ◽  
Author(s):  
Stephen R. Williams ◽  
Greg J. Stuart
Keyword(s):  
Sodium Channels ◽  
Temporal Summation ◽  
Time Course ◽  
Pyramidal Neurons ◽  
Apical Dendrite ◽  
Linear Increase ◽  
Nonuniform Distribution ◽  
Excitatory Synaptic Input ◽  
Pharmacological Blockade ◽  
Apical Dendrites

Neocortical layer 5 pyramidal neurons possess long apical dendrites that receive a significant portion of the neurons excitatory synaptic input. Passive neuronal models indicate that the time course of excitatory postsynaptic potentials (EPSPs) generated in the apical dendrite will be prolonged as they propagate toward the soma. EPSP propagation may, however, be influenced by the recruitment of dendritic voltage-activated channels. Here we investigate the properties and distribution of I h channels in the axon, soma, and apical dendrites of neocortical layer 5 pyramidal neurons, and their effect on EPSP time course. We find a linear increase (9 pA/100 μm) in the density of dendritic I hchannels with distance from soma. This nonuniform distribution of I h channels generates site independence of EPSP time course, such that the half-width at the soma of distally generated EPSPs (up to 435 μm from soma) was similar to somatically generated EPSPs. As a corollary, a normalization of temporal summation of EPSPs was observed. The site independence of somatic EPSP time course was found to collapse after pharmacological blockade of I h channels, revealing pronounced temporal summation of distally generated EPSPs, which could be further enhanced by TTX-sensitive sodium channels. These data indicate that an increasing density of apical dendritic I hchannels mitigates the influence of cable filtering on somatic EPSP time course and temporal summation in neocortical layer 5 pyramidal neurons.

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