scholarly journals Dopamine Modulates Spike Timing-Dependent Plasticity and Action Potential Properties in CA1 Pyramidal Neurons of Acute Rat Hippocampal Slices

2011 ◽  
Vol 3 ◽  
Author(s):  
Elke Edelmann ◽  
Volkmar Lessmann
Keyword(s):  
Action Potential ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Ca1 Pyramidal Neurons

Influence of acetylcholine on spike timing-dependent plasticity in CA1 network of rat hippocampal slices

2011 ◽  
Vol 71 ◽  
pp. e111-e112
Author(s):  
Eriko Sugisaki ◽  
Yasuhiro Fukushima ◽  
Hirofumi Hayakawa ◽  
Minoru Tsukada ◽  
Takeshi Aihara
Keyword(s):  
Hippocampal Slices ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity

scholarly journals Development of dendritic tonic GABAergic inhibition regulates excitability and plasticity in CA1 pyramidal neurons

2014 ◽  
Vol 112 (2) ◽  
pp. 287-299 ◽  
Author(s):  
Martine R. Groen ◽  
Ole Paulsen ◽  
Enrique Pérez-Garci ◽  
Thomas Nevian ◽  
J. Wortel ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Action Potential ◽  
Pyramidal Neurons ◽  
Spike Timing ◽  
Tonic Inhibition ◽  
Developmental Changes ◽  
Gabaergic Inhibition ◽  
Gaba A ◽  
Ca1 Pyramidal Neurons ◽  
Mature Neurons

Synaptic plasticity rules change during development: while hippocampal synapses can be potentiated by a single action potential pairing protocol in young neurons, mature neurons require burst firing to induce synaptic potentiation. An essential component for spike timing-dependent plasticity is the backpropagating action potential (BAP). BAP along the dendrites can be modulated by morphology and ion channel composition, both of which change during late postnatal development. However, it is unclear whether these dendritic changes can explain the developmental changes in synaptic plasticity induction rules. Here, we show that tonic GABAergic inhibition regulates dendritic action potential backpropagation in adolescent, but not preadolescent, CA1 pyramidal neurons. These developmental changes in tonic inhibition also altered the induction threshold for spike timing-dependent plasticity in adolescent neurons. This GABAergic regulatory effect on backpropagation is restricted to distal regions of apical dendrites (>200 μm) and mediated by α5-containing GABA(A) receptors. Direct dendritic recordings demonstrate α5-mediated tonic GABA(A) currents in adolescent neurons which can modulate BAPs. These developmental modulations in dendritic excitability could not be explained by concurrent changes in dendritic morphology. To explain our data, model simulations propose a distally increasing or localized distal expression of dendritic α5 tonic inhibition in mature neurons. Overall, our results demonstrate that dendritic integration and plasticity in more mature dendrites are significantly altered by tonic α5 inhibition in a dendritic region-specific and developmentally regulated manner.

Role of AMPA and NMDA Receptors and Back-Propagating Action Potentials in Spike Timing–Dependent Plasticity

2010 ◽  
Vol 103 (1) ◽  
pp. 47-54 ◽  
Author(s):  
Marco Fuenzalida ◽  
David Fernández de Sevilla ◽  
Alejandro Couve ◽  
Washington Buño
Keyword(s):  
Nmda Receptors ◽  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Cellular Mechanisms ◽  
Dependent Plasticity ◽  
Term Potentiation

The cellular mechanisms that mediate spike timing–dependent plasticity (STDP) are largely unknown. We studied in vitro in CA1 pyramidal neurons the contribution of AMPA and N-methyl-d-aspartate (NMDA) components of Schaffer collateral (SC) excitatory postsynaptic potentials (EPSPs; EPSPAMPA and EPSPNMDA) and of the back-propagating action potential (BAP) to the long-term potentiation (LTP) induced by a STDP protocol that consisted in pairing an EPSP and a BAP. Transient blockade of EPSPAMPA with 7-nitro-2,3-dioxo-1,4-dihydroquinoxaline-6-carbonitrile (CNQX) during the STDP protocol prevented LTP. Contrastingly LTP was induced under transient inhibition of EPSPAMPA by combining SC stimulation, an imposed EPSPAMPA-like depolarization, and BAP or by coupling the EPSPNMDA evoked under sustained depolarization (approximately −40 mV) and BAP. In Mg2+-free solution EPSPNMDA and BAP also produced LTP. Suppression of EPSPNMDA or BAP always prevented LTP. Thus activation of NMDA receptors and BAPs are needed but not sufficient because AMPA receptor activation is also obligatory for STDP. However, a transient depolarization of another origin that unblocks NMDA receptors and a BAP may also trigger LTP.

scholarly journals A spike-timing-dependent plasticity rule for single, clustered and distributed dendritic spines

2018 ◽  
Author(s):  
Sabrina Tazerart ◽  
Diana E. Mitchell ◽  
Soledad Miranda-Rottmann ◽  
Roberto Araya
Keyword(s):  
Dendritic Spines ◽  
Actin Polymerization ◽  
Pyramidal Neurons ◽  
Glutamate Release ◽  
Synaptic Strength ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Spine Shape ◽  
Stdp Rule

SUMMARYSpike-timing-dependent plasticity (STDP) has been extensively studied in cortical pyramidal neurons, however, the precise structural organization of excitatory inputs that supports STDP, as well as the structural, molecular and functional properties of dendritic spines during STDP remain unknown. Here we performed a spine STDP protocol using two-photon glutamate uncaging to mimic presynaptic glutamate release (pre) paired with somatically generated postsynaptic spikes (post). We found that the induction of STDP in single spines follows a classical Hebbian STDP rule, where pre-post pairings at timings that trigger LTP (t-LTP) produce shrinkage of the activated spine neck and a concomitant increase in its synaptic strength; and post-pre pairings that trigger LTD (t-LTD) decrease synaptic strength without affecting the activated spine shape. Furthermore, we tested whether the single spine-Hebbian STDP rule could be affected by the activation of neighboring (clustered) or distant (distributed) spines. Our results show that the induction of t-LTP in two clustered spines (<5 μm apart) enhances LTP through a mechanism dependent on local spine calcium accumulation and actin polymerization-dependent neck shrinkage, whereas t-LTD was disrupted by the activation of two clustered spines but recovered when spines were separated by >40 μm. These results indicate that synaptic cooperativity, induced by the co-activation of only two clustered spines, provides local dendritic depolarization and local calcium signals sufficient to disrupt t-LTD and extend the temporal window for the induction of t-LTP, leading to STDP only encompassing LTP.

scholarly journals Impairment of Spike-Timing-Dependent Plasticity at Schaffer Collateral-CA1 Synapses in Adult APP/PS1 Mice Depends on Proximity of Aβ Plaques

2021 ◽  
Vol 22 (3) ◽  
pp. 1378
Author(s):  
Machhindra Garad ◽  
Elke Edelmann ◽  
Volkmar Leßmann
Keyword(s):  
Neurodegenerative Disorder ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
Dependent Manner ◽  
Spike Timing Dependent Plasticity ◽  
Schaffer Collateral ◽  
Ca1 Neurons ◽  
Dependent Plasticity ◽  
The Impact

Alzheimer’s disease (AD) is a multifaceted neurodegenerative disorder characterized by progressive and irreversible cognitive decline, with no disease-modifying therapy until today. Spike timing-dependent plasticity (STDP) is a Hebbian form of synaptic plasticity, and a strong candidate to underlie learning and memory at the single neuron level. Although several studies reported impaired long-term potentiation (LTP) in the hippocampus in AD mouse models, the impact of amyloid-β (Aβ) pathology on STDP in the hippocampus is not known. Using whole cell patch clamp recordings in CA1 pyramidal neurons of acute transversal hippocampal slices, we investigated timing-dependent (t-) LTP induced by STDP paradigms at Schaffer collateral (SC)-CA1 synapses in slices of 6-month-old adult APP/PS1 AD model mice. Our results show that t-LTP can be induced even in fully developed adult mice with different and even low repeat STDP paradigms. Further, adult APP/PS1 mice displayed intact t-LTP induced by 1 presynaptic EPSP paired with 4 postsynaptic APs (6× 1:4) or 1 presynaptic EPSP paired with 1 postsynaptic AP (100× 1:1) STDP paradigms when the position of Aβ plaques relative to recorded CA1 neurons in the slice were not considered. However, when Aβ plaques were live stained with the fluorescent dye methoxy-X04, we observed that in CA1 neurons with their somata <200 µm away from the border of the nearest Aβ plaque, t-LTP induced by 6× 1:4 stimulation was significantly impaired, while t-LTP was unaltered in CA1 neurons >200 µm away from plaques. Treatment of APP/PS1 mice with the anti-inflammatory drug fingolimod that we previously showed to alleviate synaptic deficits in this AD mouse model did not rescue the impaired t-LTP. Our data reveal that overexpression of APP and PS1 mutations in AD model mice disrupts t-LTP in an Aβ plaque distance-dependent manner, but cannot be improved by fingolimod (FTY720) that has been shown to rescue conventional LTP in CA1 of APP/PS1 mice.

scholarly journals Activation of Ih and TTX-sensitive sodium current at subthreshold voltages during CA1 pyramidal neuron firing

2015 ◽  
Vol 114 (4) ◽  
pp. 2376-2389 ◽  
Author(s):  
Jason Yamada-Hanff ◽  
Bruce P. Bean
Keyword(s):  
Action Potential ◽  
Time Constant ◽  
Pyramidal Neurons ◽  
Sodium Current ◽  
Hippocampal Slices ◽  
Input Resistance ◽  
Hcn Channels ◽  
Dynamic Clamp ◽  
Ca1 Neurons ◽  
Ca1 Pyramidal Neurons

We used dynamic clamp and action potential clamp techniques to explore how currents carried by tetrodotoxin-sensitive sodium channels and HCN channels ( Ih) regulate the behavior of CA1 pyramidal neurons at resting and subthreshold voltages. Recording from rat CA1 pyramidal neurons in hippocampal slices, we found that the apparent input resistance and membrane time constant were strongly affected by both conductances, with Ih acting to decrease apparent input resistance and time constant and sodium current acting to increase both. We found that both Ih and sodium current were active during subthreshold summation of artificial excitatory postsynaptic potentials (EPSPs) generated by dynamic clamp, with Ih dominating at less depolarized voltages and sodium current at more depolarized voltages. Subthreshold sodium current—which amplifies EPSPs—was most effectively recruited by rapid voltage changes, while Ih—which blunts EPSPs—was maximal for slow voltage changes. The combined effect is to selectively amplify rapid EPSPs. We did similar experiments in mouse CA1 pyramidal neurons, doing voltage-clamp experiments using experimental records of action potential firing of CA1 neurons previously recorded in awake, behaving animals as command voltages to quantify flow of Ih and sodium current at subthreshold voltages. Subthreshold sodium current was larger and subthreshold Ih was smaller in mouse neurons than in rat neurons. Overall, the results show opposing effects of subthreshold sodium current and Ih in regulating subthreshold behavior of CA1 neurons, with subthreshold sodium current prominent in both rat and mouse CA1 pyramidal neurons and additional regulation by Ih in rat neurons.

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