scholarly journals Open Up to Make New Contacts: Caldendrin Senses Postsynaptic Calcium Influx to Dynamically Organize Dendritic Spines

Neuron ◽  
2018 ◽  
Vol 97 (5) ◽  
pp. 994-996
Author(s):  
Andrew Coleman ◽  
Thomas Biederer
Keyword(s):  
Dendritic Spines ◽  
Calcium Influx ◽  
Postsynaptic Calcium

scholarly journals L-Type Calcium Channels Are Required for One Form of Hippocampal Mossy Fiber LTP

1998 ◽  
Vol 79 (4) ◽  
pp. 2181-2190 ◽  
Author(s):  
Ajay Kapur ◽  
Mark F. Yeckel ◽  
Richard Gray ◽  
Daniel Johnston
Keyword(s):  
Calcium Channels ◽  
High Frequency ◽  
Pyramidal Neurons ◽  
Mossy Fiber ◽  
Calcium Influx ◽  
Calcium Transients ◽  
High Frequency Stimulation ◽  
Frequency Stimulation ◽  
Ca3 Pyramidal Neurons ◽  
Postsynaptic Calcium

Kapur, Ajay, Mark F. Yeckel, Richard Gray, and Daniel Johnston. L-type calcium channels are required for one form of hippocampal mossy fiber LTP. J. Neurophysiol. 79: 2181–2190, 1998. The requirement of postsynaptic calcium influx via L-type channels for the induction of long-term potentiation (LTP) of mossy fiber input to CA3 pyramidal neurons was tested for two different patterns of stimulation. Two types of LTP-inducing stimuli were used based on the suggestion that one of them, brief high-frequency stimulation (B-HFS), induces LTP postsynaptically, whereas the other pattern, long high-frequency stimulation (L-HFS), induces mossy fiber LTP presynaptically. To test whether or not calcium influx into CA3 pyramidal neurons is necessary for LTP induced by either pattern of stimulation, nimodipine, a L-type calcium channel antagonist, was added during stimulation. In these experiments nimodipine blocked the induction of mossy fiber LTP when B-HFS was given [34 ± 5% (mean ± SE) increase in control versus 7 ± 4% in nimodipine, P < 0.003]; in contrast, nimodipine did not block the induction of LTP with L-HFS (107 ± 10% in control vs. 80 ± 9% in nimodipine, P > 0.05). Administration of nimodipine after the induction of LTP had no effect on the expression of LTP. In addition, B- and L-HFS delivered directly to commissural/associational fibers in stratum radiatum failed to induce a N-methyl-d-aspartate-independent form of LTP, obviating the possibility that the presumed mossy fiber LTP resulted from potentiation of other synapses. Nimodipine had no effect on calcium transients recorded from mossy fiber presynaptic terminals evoked with the B-HFS paradigm but reduced postsynaptic calcium transients. Our results support the hypothesis that induction of mossy fiber LTP by B-HFS is mediated postsynaptically and requires entry of calcium through L-type channels into CA3 neurons.

scholarly journals Evidence of calcium-permeable AMPA receptors in dendritic spines of CA1 pyramidal neurons

2014 ◽  
Vol 112 (2) ◽  
pp. 263-275 ◽  
Author(s):  
Hayley A. Mattison ◽  
Ashish A. Bagal ◽  
Michael Mohammadi ◽  
Nisha S. Pulimood ◽  
Christian G. Reich ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Ampa Receptors ◽  
Pyramidal Neurons ◽  
Calcium Influx ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Stratum Radiatum ◽  
Acute Hippocampal Slices ◽  
Cultured Slices ◽  
Apical Dendrites

GluA2-lacking, calcium-permeable α-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors (AMPARs) have unique properties, but their presence at excitatory synapses in pyramidal cells is controversial. We have tested certain predictions of the model that such receptors are present in CA1 cells and show here that the polyamine spermine, but not philanthotoxin, causes use-dependent inhibition of synaptically evoked excitatory responses in stratum radiatum, but not s. oriens, in cultured and acute hippocampal slices. Stimulation of single dendritic spines by photolytic release of caged glutamate induced an N-methyl-d-aspartate receptor-independent, use- and spermine-sensitive calcium influx only at apical spines in cultured slices. Bath application of glutamate also triggered a spermine-sensitive influx of cobalt into CA1 cell dendrites in s. radiatum. Responses of single apical, but not basal, spines to photostimulation displayed prominent paired-pulse facilitation (PPF) consistent with use-dependent relief of cytoplasmic polyamine block. Responses at apical dendrites were diminished, and PPF was increased, by spermine. Intracellular application of pep2m, which inhibits recycling of GluA2-containing AMPARs, reduced apical spine responses and increased PPF. We conclude that some calcium-permeable, polyamine-sensitive AMPARs, perhaps lacking GluA2 subunits, are present at synapses on apical dendrites of CA1 pyramidal cells, which may allow distinct forms of synaptic plasticity and computation at different sets of excitatory inputs.

NMDA receptors amplify calcium influx into dendritic spines during associative pre- and postsynaptic activation

10.1038/363 ◽  
1998 ◽  
Vol 1 (2) ◽  
pp. 114-118 ◽  
Author(s):  
Jackie Schiller ◽  
Yitzhak Schiller ◽  
David E. Clapham
Keyword(s):  
Nmda Receptors ◽  
Dendritic Spines ◽  
Calcium Influx

scholarly journals Paradoxical signaling regulates structural plasticity in dendritic spines

2016 ◽  
Vol 113 (36) ◽  
pp. E5298-E5307 ◽  
Author(s):  
Padmini Rangamani ◽  
Michael G. Levy ◽  
Shahid Khan ◽  
George Oster
Keyword(s):  
Dendritic Spines ◽  
Molecular Mechanisms ◽  
Calcium Influx ◽  
Structural Plasticity ◽  
Receptor Activation ◽  
Protein Activity ◽  
Actin Remodeling ◽  
Dependent Protein ◽  
Nmda Receptor Activation

Transient spine enlargement (3- to 5-min timescale) is an important event associated with the structural plasticity of dendritic spines. Many of the molecular mechanisms associated with transient spine enlargement have been identified experimentally. Here, we use a systems biology approach to construct a mathematical model of biochemical signaling and actin-mediated transient spine expansion in response to calcium influx caused by NMDA receptor activation. We have identified that a key feature of this signaling network is the paradoxical signaling loop. Paradoxical components act bifunctionally in signaling networks, and their role is to control both the activation and the inhibition of a desired response function (protein activity or spine volume). Using ordinary differential equation (ODE)-based modeling, we show that the dynamics of different regulators of transient spine expansion, including calmodulin-dependent protein kinase II (CaMKII), RhoA, and Cdc42, and the spine volume can be described using paradoxical signaling loops. Our model is able to capture the experimentally observed dynamics of transient spine volume. Furthermore, we show that actin remodeling events provide a robustness to spine volume dynamics. We also generate experimentally testable predictions about the role of different components and parameters of the network on spine dynamics.

scholarly journals Nanoscale organization and calcium influx in dendritic spines guarantee ER store refilling without depletion

2021 ◽  
Author(s):  
Kanishka Basnayake ◽  
David Mazaud ◽  
Lilia Kushnireva ◽  
Alexis Bemelmans ◽  
nathalie Rouach ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Plasma Membranes ◽  
Calcium Release ◽  
Calcium Influx ◽  
Smooth Endoplasmic Reticulum ◽  
Super Resolution ◽  
Calcium Stores ◽  
Calcium Dynamics ◽  
Store Operated Calcium Entry ◽  
Critical Components

Dendritic spines are critical components of the neuronal synapse as they receive and transform the synaptic input into a succession of biochemical events regulated by calcium signaling. The spine apparatus (SA), an extension of smooth endoplasmic reticulum (ER), regulates slow and fast calcium dynamics in spines. Calcium release events from SA result in a rapid depletion of calcium ion reservoir, yet the next cycle of signaling requires replenishment of SA calcium stores. How dendritic spines achieve this without triggering calcium release remains unclear. Using computational modeling, calcium and STED super-resolution imaging, we showed that the refilling of calcium-deprived SA involves store-operated calcium entry during spontaneous calcium transients in spine heads. We identified two main conditions that guarantee SA replenishment without depletion: (1) a small amplitude and slow timescale for calcium influx, and (2) a close proximity between SA and plasma membranes. Thereby, molecular nano-organization creates the conditions for a clear separation between SA replenishment and depletion. We further conclude that the nanoscale organization of SA receptors underlies the specificity of calcium dynamics patterns during the induction of long-term synaptic changes.

scholarly journals Spatiotemporal Dynamics of Calmodulin in Dendritic Spines during Calcium Influx

2013 ◽  
Vol 104 (2) ◽  
pp. 163a-164a ◽  
Author(s):  
Matyas Matolcsi ◽  
Nicholas Giordano
Keyword(s):  
Dendritic Spines ◽  
Calcium Influx ◽  
Spatiotemporal Dynamics

scholarly journals Paradoxical signaling regulates structural plasticity in dendritic spines

2016 ◽  
Author(s):  
Padmini Rangamani ◽  
Michael G. Levy ◽  
Shahid M. Khan ◽  
George Oster
Keyword(s):  
Differential Equation ◽  
Dendritic Spines ◽  
Molecular Mechanisms ◽  
Calcium Influx ◽  
Structural Plasticity ◽  
Receptor Activation ◽  
Protein Activity ◽  
Nmda Receptor Activation ◽  
Spine Dynamics

AbstractTransient spine enlargement (3-5 min timescale) is an important event associated with the structural plasticity of dendritic spines. Many of the molecular mechanisms associated with transient spine en­largement have been identified experimentally. Here, we use a systems biology approach to construct a mathematical model of biochemical signaling and actin-mediated transient spine expansion in response to calcium-influx due to NMDA receptor activation. We have identified that a key feature of this signaling network is the paradoxical signaling loop. Paradoxical components act bifunctionally in signaling net­works and their role is to control both the activation and inhibition of a desired response function (protein activity or spine volume). Using ordinary differential equation (ODE)-based modeling, we show that the dynamics of different regulators of transient spine expansion including CaMKII, RhoA, and Cdc42 and the spine volume can be described using paradoxical signaling loops. Our model is able to capture the experimentally observed dynamics of transient spine volume. Furthermore, we show that actin remod­eling events provide a robustness to spine volume dynamics. We also generate experimentally testable predictions about the role of different components and parameters of the network on spine dynamics.

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