scholarly journals Synaptic Plasticity in vivo: More than Just Spike-Timing?

2010 ◽  
Vol 2 ◽  
Author(s):  
Jan M. Schulz
Keyword(s):  
Synaptic Plasticity ◽  
Spike Timing

scholarly journals Dynamic modulation of spike timing-dependent calcium influx during corticostriatal upstates

2013 ◽  
Vol 110 (7) ◽  
pp. 1631-1645 ◽  
Author(s):  
R. C. Evans ◽  
Y. M. Maniar ◽  
K. T. Blackwell
Keyword(s):  
Synaptic Plasticity ◽  
Slow Wave Sleep ◽  
Calcium Influx ◽  
Spike Timing ◽  
Medium Spiny Neuron ◽  
Calcium Transients ◽  
Biophysical Model ◽  
Published Data ◽  
High Calcium

The striatum of the basal ganglia demonstrates distinctive upstate and downstate membrane potential oscillations during slow-wave sleep and under anesthetic. The upstates generate calcium transients in the dendrites, and the amplitude of these calcium transients depends strongly on the timing of the action potential (AP) within the upstate. Calcium is essential for synaptic plasticity in the striatum, and these large calcium transients during the upstates may control which synapses undergo plastic changes. To investigate the mechanisms that underlie the relationship between calcium and AP timing, we have developed a realistic biophysical model of a medium spiny neuron (MSN). We have implemented sophisticated calcium dynamics including calcium diffusion, buffering, and pump extrusion, which accurately replicate published data. Using this model, we found that either the slow inactivation of dendritic sodium channels (NaSI) or the calcium inactivation of voltage-gated calcium channels (CDI) can cause high calcium corresponding to early APs and lower calcium corresponding to later APs. We found that only CDI can account for the experimental observation that sensitivity to AP timing is dependent on NMDA receptors. Additional simulations demonstrated a mechanism by which MSNs can dynamically modulate their sensitivity to AP timing and show that sensitivity to specifically timed pre- and postsynaptic pairings (as in spike timing-dependent plasticity protocols) is altered by the timing of the pairing within the upstate. These findings have implications for synaptic plasticity in vivo during sleep when the upstate-downstate pattern is prominent in the striatum.

scholarly journals Reconciling the STDP and BCM Models of Synaptic Plasticity in a Spiking Recurrent Neural Network

2010 ◽  
Vol 22 (8) ◽  
pp. 2059-2085 ◽  
Author(s):  
Daniel Bush ◽  
Andrew Philippides ◽  
Phil Husbands ◽  
Michael O'Shea
Keyword(s):  
Neural Network ◽  
Synaptic Plasticity ◽  
Recurrent Neural Network ◽  
Hebbian Learning ◽  
Spike Timing ◽  
Synaptic Competition ◽  
Firing Rates ◽  
Plasticity Rule ◽  
Asymmetric Learning

Rate-coded Hebbian learning, as characterized by the BCM formulation, is an established computational model of synaptic plasticity. Recently it has been demonstrated that changes in the strength of synapses in vivo can also depend explicitly on the relative timing of pre- and postsynaptic firing. Computational modeling of this spike-timing-dependent plasticity (STDP) has demonstrated that it can provide inherent stability or competition based on local synaptic variables. However, it has also been demonstrated that these properties rely on synaptic weights being either depressed or unchanged by an increase in mean stochastic firing rates, which directly contradicts empirical data. Several analytical studies have addressed this apparent dichotomy and identified conditions under which distinct and disparate STDP rules can be reconciled with rate-coded Hebbian learning. The aim of this research is to verify, unify, and expand on these previous findings by manipulating each element of a standard computational STDP model in turn. This allows us to identify the conditions under which this plasticity rule can replicate experimental data obtained using both rate and temporal stimulation protocols in a spiking recurrent neural network. Our results describe how the relative scale of mean synaptic weights and their dependence on stochastic pre- or postsynaptic firing rates can be manipulated by adjusting the exact profile of the asymmetric learning window and temporal restrictions on spike pair interactions respectively. These findings imply that previously disparate models of rate-coded autoassociative learning and temporally coded heteroassociative learning, mediated by symmetric and asymmetric connections respectively, can be implemented in a single network using a single plasticity rule. However, we also demonstrate that forms of STDP that can be reconciled with rate-coded Hebbian learning do not generate inherent synaptic competition, and thus some additional mechanism is required to guarantee long-term input-output selectivity.

scholarly journals Modulation of Synaptic Plasticity by Glutamatergic Gliotransmission: A Modeling Study

2016 ◽  
Vol 2016 ◽  
pp. 1-30 ◽  
Author(s):  
Maurizio De Pittà ◽  
Nicolas Brunel
Keyword(s):  
Synaptic Plasticity ◽  
Glutamate Release ◽  
Spike Timing ◽  
Biophysical Model ◽  
Dependent Manner ◽  
Inward Currents ◽  
Functional Relevance ◽  
And Function ◽  
Activity Dependent

Glutamatergic gliotransmission, that is, the release of glutamate from perisynaptic astrocyte processes in an activity-dependent manner, has emerged as a potentially crucial signaling pathway for regulation of synaptic plasticity, yet its modes of expression and function in vivo remain unclear. Here, we focus on two experimentally well-identified gliotransmitter pathways, (i) modulations of synaptic release and (ii) postsynaptic slow inward currents mediated by glutamate released from astrocytes, and investigate their possible functional relevance on synaptic plasticity in a biophysical model of an astrocyte-regulated synapse. Our model predicts that both pathways could profoundly affect both short- and long-term plasticity. In particular, activity-dependent glutamate release from astrocytes could dramatically change spike-timing-dependent plasticity, turning potentiation into depression (and vice versa) for the same induction protocol.

scholarly journals Synaptic plasticity is predicted by spatiotemporal firing rate patterns and robust to in vivo-like variability

2021 ◽  
Author(s):  
Dan B Dorman ◽  
Kim T Blackwell
Keyword(s):  
Synaptic Plasticity ◽  
Firing Rate ◽  
Dendritic Tree ◽  
Spike Timing ◽  
Synaptic Activity ◽  
Data Driven ◽  
Synaptic Inputs ◽  
The Brain

Synaptic plasticity, the experience-induced change in connections between neurons, underlies learning and memory in the brain. Most of our understanding of synaptic plasticity derives from in vitro experiments with precisely repeated stimulus patterns; however, neurons exhibit significant variability in vivo during repeated experiences. Further, the spatial pattern of synaptic inputs to the dendritic tree influences synaptic plasticity, yet is not considered in most synaptic plasticity rules. Here, we address the sensitivity of plasticity to trial-to-trial variability and delineate how spatiotemporal synaptic input patterns produce plasticity with in vivo-like conditions using a data-driven computational model with a calcium-based plasticity rule. Using in vivo spike train recordings as inputs, we show that plasticity is strongly robust to trial-to-trial variability of spike timing, and derive general synaptic plasticity rules describing how spatiotemporal patterns of synaptic inputs control the magnitude and direction of plasticity. Specifically, a high temporal input firing rate to a synapse late in a trial correlated with neighboring synaptic activity produces potentiation, while an earlier, moderate firing rate that is negatively correlated with neighboring synaptic activity produces depression. Together, our results reveal that calcium dynamics can unify diverse plasticity rules and reveal how spatiotemporal firing rate patterns control synaptic plasticity.

scholarly journals Calcium and Spike Timing-Dependent Plasticity

2021 ◽  
Vol 15 ◽  
Author(s):  
Yanis Inglebert ◽  
Dominique Debanne
Keyword(s):  
Synaptic Plasticity ◽  
Calcium Concentration ◽  
Calcium Influx ◽  
Spike Timing ◽  
Extracellular Calcium ◽  
Dependent Plasticity ◽  
Extracellular Calcium Concentration ◽  
Activity Dependent

Since its discovery, spike timing-dependent synaptic plasticity (STDP) has been thought to be a primary mechanism underlying the brain’s ability to learn and to form new memories. However, despite the enormous interest in both the experimental and theoretical neuroscience communities in activity-dependent plasticity, it is still unclear whether plasticity rules inferred from in vitro experiments apply to in vivo conditions. Among the multiple reasons why plasticity rules in vivo might differ significantly from in vitro studies is that extracellular calcium concentration use in most studies is higher than concentrations estimated in vivo. STDP, like many forms of long-term synaptic plasticity, strongly depends on intracellular calcium influx for its induction. Here, we discuss the importance of considering physiological levels of extracellular calcium concentration to study functional plasticity.

scholarly journals Locally coordinated synaptic plasticity shapes cell-wide plasticity of visual cortex neurons in vivo

2018 ◽  
Author(s):  
Sami El-Boustani ◽  
Jacque P K Ip ◽  
Vincent Breton-Provencher ◽  
Hiroyuki Okuno ◽  
Haruhiko Bito ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Visual Cortex ◽  
Spike Timing ◽  
Monocular Deprivation ◽  
Early Gene ◽  
Neuronal Responses ◽  
Functional Changes ◽  
Targeted Expression ◽  
Visual Cortex Neurons

AbstractPlasticity of cortical responses involves activity-dependent changes at synapses, but the manner in which different forms of synaptic plasticity act together to create functional changes in neuronal responses remains unknown. Here we show that spike-timing induced receptive field plasticity of individual visual cortex neurons in vivo is anchored by increases in synaptic strength of identified spines, and is accompanied by a novel decrease in the strength of adjacent spines on a slower time scale. The locally coordinated potentiation and depression of spines involves prominent AMPA receptor redistribution via targeted expression of the immediate early gene Arc. Similar changes accompany recovery of eye-specific responses following monocular deprivation. These findings demonstrate that Hebbian strengthening of activated synapses and heterosynaptic weakening of adjacent synapses, in dendrites with heterogeneous synaptic inputs, co-operatively orchestrate cell-wide plasticity of functional neuronal responses.One Sentence SummaryArc-mediated local synaptic plasticity regulates reorganization of synaptic responses on dendritic stretches to mediate functional plasticity of neuronal responses in vivo.

scholarly journals Chronic mild stress alters synaptic plasticity in the nucleus accumbens through GSK3β-dependent modulation of Kv4.2 channels

2020 ◽  
Vol 117 (14) ◽  
pp. 8143-8153 ◽  
Author(s):  
Giuseppe Aceto ◽  
Claudia Colussi ◽  
Lucia Leone ◽  
Salvatore Fusco ◽  
Marco Rinaudo ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Nucleus Accumbens ◽  
Viral Vector ◽  
Glycogen Synthase ◽  
Chronic Mild Stress ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
Mild Stress

Although major depressive disorder (MDD) is highly prevalent, its pathophysiology is poorly understood. Recent evidence suggests that glycogen-synthase kinase 3β (GSK3β) plays a key role in memory formation, yet its role in mood regulation remains controversial. Here, we investigated whether GSK3β activity in the nucleus accumbens (NAc) is associated with depression-like behaviors and synaptic plasticity. We performed whole-cell patch-clamp recordings of medium spiny neurons (MSNs) in the NAc and determined the role of GSK3β in spike timing-dependent long-term potentiation (tLTP) in the chronic unpredictable mild stress (CUMS) mouse model of depression. To assess the specific role of GSK3β in tLTP, we used in vivo genetic silencing by an adeno-associated viral vector (AAV2) short hairpin RNA against GSK3β. In addition, we examined the role of the voltage-gated potassium Kv4.2 subunit, a molecular determinant of A-type K+currents, as a potential downstream target of GSK3β. We found increased levels of active GSK3β and augmented tLTP in CUMS mice, a phenotype that was prevented by selective GSK3β knockdown. Furthermore, knockdown of GSK3β in the NAc ameliorated depressive-like behavior in CUMS mice. Electrophysiological, immunohistochemical, biochemical, and pharmacological experiments revealed that inhibition of the Kv4.2 channel through direct phosphorylation at Ser-616 mediated the GSK3β-dependent tLTP changes in CUMS mice. Our results identify GSK3β regulation of Kv4.2 channels as a molecular mechanism of MSN maladaptive plasticity underlying depression-like behaviors and suggest that the GSK3β–Kv4.2 axis may be an attractive therapeutic target for MDD.

scholarly journals A stochastic model of hippocampal synaptic plasticity with geometrical readout of enzyme dynamics

2021 ◽  
Author(s):  
Yuri Elias Rodrigues ◽  
Cezar M. Tigaret ◽  
Hélène Marie ◽  
Cian O'Donnell ◽  
Romain Veltz
Keyword(s):  
Synaptic Plasticity ◽  
Computational Models ◽  
Ex Vivo ◽  
Extracellular Fluid ◽  
Intrinsic Noise ◽  
Spike Timing ◽  
Fluid Composition ◽  
Enzyme Dynamics ◽  
Experimental Conditions

Synaptic plasticity rules used in current computational models of learning are generally insensitive to physiological factors such as spine voltage, animal age, extracellular fluid composition, and body temperature, limiting their predictive power. Here, we built a biophysically detailed synapse model inclusive of electrical dynamics, calcium-dependent signaling via CaMKII and Calcineurin (CaN) activities. The model combined multi-timescale variables, milliseconds to minutes, and intrinsic noise from stochastic ion channel gating. Analysis of the trajectories of joint CaMKII and CaN activities yielded an interpretable geometrical readout that fitted the synaptic plasticity outcomes of nine published ex vivo experiments covering various spike-timing and frequency-dependent plasticity induction protocols, animal ages, and experimental conditions. Using this new approach, we then generated maps predicting plasticity outcomes across the space of these stimulation conditions. Finally, we tested the model's robustness to in vivo-like spike time irregularity, showing that it significantly alters plasticity outcomes.

scholarly journals Locally coordinated synaptic plasticity of visual cortex neurons in vivo

Science ◽  
2018 ◽  
Vol 360 (6395) ◽  
pp. 1349-1354 ◽  
Author(s):  
Sami El-Boustani ◽  
Jacque P. K. Ip ◽  
Vincent Breton-Provencher ◽  
Graham W. Knott ◽  
Hiroyuki Okuno ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Visual Cortex ◽  
Spike Timing ◽  
Early Gene ◽  
Functional Changes ◽  
Cortical Responses ◽  
Targeted Expression ◽  
Visual Cortex Neurons ◽  
Activity Dependent

Plasticity of cortical responses in vivo involves activity-dependent changes at synapses, but the manner in which different forms of synaptic plasticity act together to create functional changes in neurons remains unknown. We found that spike timing–induced receptive field plasticity of visual cortex neurons in mice is anchored by increases in the synaptic strength of identified spines. This is accompanied by a decrease in the strength of adjacent spines on a slower time scale. The locally coordinated potentiation and depression of spines involves prominent AMPA receptor redistribution via targeted expression of the immediate early gene product Arc. Hebbian strengthening of activated synapses and heterosynaptic weakening of adjacent synapses thus cooperatively orchestrate cell-wide plasticity of functional neuronal responses.

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