scholarly journals Bidirectional synaptic plasticity rapidly modifies hippocampal representations independent of correlated activity

2020 ◽  
Author(s):  
Aaron D. Milstein ◽  
Yiding Li ◽  
Katie C. Bittner ◽  
Christine Grienberger ◽  
Ivan Soltesz ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Network Modeling ◽  
Place Cells ◽  
Synaptic Activity ◽  
Associative Memories ◽  
Population Activity ◽  
Correlated Activity ◽  
Dependent Model ◽  
Standard Models

AbstractAccording to standard models of synaptic plasticity, correlated activity between connected neurons drives changes in synaptic strengths to store associative memories. Here we tested this hypothesis in vivo by manipulating the activity of hippocampal place cells and measuring the resulting changes in spatial selectivity. We found that the spatial tuning of place cells was rapidly reshaped via bidirectional synaptic plasticity. To account for the magnitude and direction of plasticity, we evaluated two models – a standard model that depended on synchronous pre- and post-synaptic activity, and an alternative model that depended instead on whether active synaptic inputs had previously been potentiated. While both models accounted equally well for the data, they predicted opposite outcomes of a perturbation experiment, which ruled out the standard correlation-dependent model. Finally, network modeling suggested that this form of bidirectional synaptic plasticity enables population activity, rather than pairwise neuronal correlations, to drive plasticity in response to changes in the environment.

scholarly journals Changes in Synaptic Terminal Structure in Adolescent Rat during Pregnancy; The Action Potential Propagation and Synaptic Transmission

2020 ◽  
pp. 1-8
Keyword(s):  
Synaptic Plasticity ◽  
Laser Scanning ◽  
Structural Changes ◽  
Specific Pattern ◽  
Laser Scanning Microscopy ◽  
Synaptic Activity ◽  
Two Photon ◽  
Sensory Experiences ◽  
Terminal Structure

Synaptic plasticity is a biological system of specific pattern of synaptic activity result in changes in synaptic strength. This influence puberty, pregnancy hormones, sensory experiences, and brain disorders. Long-term synaptic plasticity is accompanied by protein synthesis and trafficking, leading to structural changes of the synapse. Increasing evidence connects the terminal synaptic changes with potential propagation in adolescent and pregnancy. We investigate on the synaptic structural plasticity, which has mainly been studied with in vivo two photon laser scanning microscopy. We also discuss how a different type of synapses, the multicontact synapses associated with pregnancy.

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 Changes in Synaptic Terminal Structure in Adolescent Rat During Pregnancy; The Action Potential Propagation and Synaptic Transmission

2020 ◽  
Vol 05 (03) ◽  
Keyword(s):  
Synaptic Plasticity ◽  
Laser Scanning ◽  
Structural Changes ◽  
Specific Pattern ◽  
Laser Scanning Microscopy ◽  
Synaptic Activity ◽  
Two Photon ◽  
Sensory Experiences ◽  
Terminal Structure

Synaptic plasticity is a biological system of specific pattern of synaptic activity result in changes in synaptic strength. This influence puberty, pregnancy hormones, sensory experiences, and brain disorders. Long-term synaptic plasticity is accompanied by protein synthesis and trafficking, leading to structural changes of the synapse. Increasing evidence connects the terminal synaptic changes with potential propagation in adolescent and pregnancy. We investigate on the synaptic structural plasticity, which has mainly been studied with in vivo two-photon laser scanning microscopy. We also discuss how a different type of synapses, the multi-contact synapses associated with pregnancy.

scholarly journals Numerical Simulation: Fluctuation in Background Synaptic Activity Regulates Synaptic Plasticity

2021 ◽  
Vol 15 ◽  
Author(s):  
Yuto Takeda ◽  
Katsuhiko Hata ◽  
Tokio Yamazaki ◽  
Masaki Kaneko ◽  
Osamu Yokoi ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Long Term Potentiation ◽  
Synaptic Activity ◽  
Statistical Fluctuation ◽  
Noisy Environment ◽  
Term Potentiation ◽  
Synapse Model ◽  
The Brain

Synaptic plasticity is vital for learning and memory in the brain. It consists of long-term potentiation (LTP) and long-term depression (LTD). Spike frequency is one of the major components of synaptic plasticity in the brain, a noisy environment. Recently, we mathematically analyzed the frequency-dependent synaptic plasticity (FDP) in vivo and found that LTP is more likely to occur with an increase in the frequency of background synaptic activity. Meanwhile, previous studies suggest statistical fluctuation in the amplitude of background synaptic activity. Little is understood, however, about its contribution to synaptic plasticity. To address this issue, we performed numerical simulations of a calcium-based synapse model. Then, we found attenuation of the tendency to become LTD due to an increase in the fluctuation of background synaptic activity, leading to an enhancement of synaptic weight. Our result suggests that the fluctuation affects synaptic plasticity in the brain.

scholarly journals Calcium Imaging Reveals Fast Tuning Dynamics of Hippocampal Place Cells and CA1 Population Activity during Free Exploration Task in Mice

2022 ◽  
Vol 23 (2) ◽  
pp. 638
Author(s):  
Vladimir P. Sotskov ◽  
Nikita A. Pospelov ◽  
Viktor V. Plusnin ◽  
Konstantin V. Anokhin
Keyword(s):  
Neuronal Activity ◽  
Calcium Imaging ◽  
Viral Vector ◽  
Place Cells ◽  
Place Field ◽  
Population Activity ◽  
Novel Environment ◽  
Mouse Hippocampus ◽  
Place Fields

Hippocampal place cells are a well-known object in neuroscience, but their place field formation in the first moments of navigating in a novel environment remains an ill-defined process. To address these dynamics, we performed in vivo imaging of neuronal activity in the CA1 field of the mouse hippocampus using genetically encoded green calcium indicators, including the novel NCaMP7 and FGCaMP7, designed specifically for in vivo calcium imaging. Mice were injected with a viral vector encoding calcium sensor, head-mounted with an NVista HD miniscope, and allowed to explore a completely novel environment (circular track surrounded by visual cues) without any reinforcement stimuli, in order to avoid potential interference from reward-related behavior. First, we calculated the average time required for each CA1 cell to acquire its place field. We found that 25% of CA1 place fields were formed at the first arrival in the corresponding place, while the average tuning latency for all place fields in a novel environment equaled 247 s. After 24 h, when the environment was familiar to the animals, place fields formed faster, independent of retention of cognitive maps during this session. No cumulation of selectivity score was observed between these two sessions. Using dimensionality reduction, we demonstrated that the population activity of rapidly tuned CA1 place cells allowed the reconstruction of the geometry of the navigated circular maze; the distribution of reconstruction error between the mice was consistent with the distribution of the average place field selectivity score in them. Our data thus show that neuronal activity recorded with genetically encoded calcium sensors revealed fast behavior-dependent plasticity in the mouse hippocampus, resulting in the rapid formation of place fields and population activity that allowed the reconstruction of the geometry of the navigated maze.

scholarly journals Functional MRI of long-term potentiation: imaging network plasticity

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130152 ◽  
Author(s):  
Efrén Álvarez-Salvado ◽  
Vicente Pallarés ◽  
Andrea Moreno ◽  
Santiago Canals
Keyword(s):  
Synaptic Plasticity ◽  
Long Term Potentiation ◽  
Plastic Property ◽  
Cellular Level ◽  
Synaptic Activity ◽  
Long Term Memory ◽  
Cellular Mechanisms ◽  
Term Potentiation

Neurons are able to express long-lasting and activity-dependent modulations of their synapses. This plastic property supports memory and conveys an extraordinary adaptive value, because it allows an individual to learn from, and respond to, changes in the environment. Molecular and physiological changes at the cellular level as well as network interactions are required in order to encode a pattern of synaptic activity into a long-term memory. While the cellular mechanisms linking synaptic plasticity to memory have been intensively studied, those regulating network interactions have received less attention. Combining high-resolution fMRI and in vivo electrophysiology in rats, we have previously reported a functional remodelling of long-range hippocampal networks induced by long-term potentiation (LTP) of synaptic plasticity in the perforant pathway. Here, we present new results demonstrating an increased bilateral coupling in the hippocampus specifically supported by the mossy cell commissural/associational pathway in response to LTP. This fMRI-measured increase in bilateral connectivity is accompanied by potentiation of the corresponding polysynaptically evoked commissural potential in the contralateral dentate gyrus and depression of the inactive convergent commissural pathway to the ipsilateral dentate. We review these and previous findings in the broader context of memory consolidation.

Brivaracetam Prevents the Over-expression of Synaptic Vesicle Protein 2A and Rescues the Deficits of Hippocampal Long-term Potentiation In Vivo in Chronic Temporal Lobe Epilepsy Rats

2020 ◽  
Vol 17 (4) ◽  
pp. 354-360 ◽  
Author(s):  
Yu-Xing Ge ◽  
Ying-Ying Lin ◽  
Qian-Qian Bi ◽  
Yu-Juan Chen
Keyword(s):  
Synaptic Plasticity ◽  
Temporal Lobe Epilepsy ◽  
Synaptic Vesicle ◽  
Long Term Potentiation ◽  
Synaptic Dysfunction ◽  
Over Expression ◽  
Term Potentiation ◽  
Synaptic Vesicle Protein 2A

Background: Patients with temporal lobe epilepsy (TLE) usually suffer from cognitive deficits and recurrent seizures. Brivaracetam (BRV) is a novel anti-epileptic drug (AEDs) recently used for the treatment of partial seizures with or without secondary generalization. Different from other AEDs, BRV has some favorable properties on synaptic plasticity. However, the underlying mechanisms remain elusive. Objective: The aim of this study was to explore the neuroprotective mechanism of BRV on synaptic plasticity in experimental TLE rats. Methods: The effect of chronic treatment with BRV (10 mg/kg) was assessed on Pilocarpine induced TLE model through measurement of the field excitatory postsynaptic potentials (fEPSPs) in vivo. Differentially expressed synaptic vesicle protein 2A (SV2A) were identified with immunoblot. Then, fast phosphorylation of synaptosomal-associated protein 25 (SNAP-25) during long-term potentiation (LTP) induction was performed to investigate the potential roles of BRV on synaptic plasticity in the TLE model. Results: An increased level of SV2A accompanied by a depressed LTP in the hippocampus was shown in epileptic rats. Furthermore, BRV treatment continued for more than 30 days improved the over-expression of SV2A and reversed the synaptic dysfunction in epileptic rats. Additionally, BRV treatment alleviates the abnormal SNAP-25 phosphorylation at Ser187 during LTP induction in epileptic ones, which is relevant to the modulation of synaptic vesicles exocytosis and voltagegated calcium channels. Conclusion: BRV treatment ameliorated the over-expression of SV2A in the hippocampus and rescued the synaptic dysfunction in epileptic rats. These results identify the neuroprotective effect of BRV on TLE model.

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 Optogenetic Regulation of Mitochondrial Function and Synaptic Plasticity In Vivo

2019 ◽  
Vol 116 (3) ◽  
pp. 267a
Author(s):  
Kristian M. Zapata ◽  
Illya Aronskyy ◽  
Stephen Madamba ◽  
Pablo M. Peixoto
Keyword(s):  
Synaptic Plasticity ◽  
Mitochondrial Function

scholarly journals Protein kinase D promotes plasticity-induced F-actin stabilization in dendritic spines and regulates memory formation

2015 ◽  
Vol 210 (5) ◽  
pp. 771-783 ◽  
Author(s):  
Norbert Bencsik ◽  
Zsófia Szíber ◽  
Hanna Liliom ◽  
Krisztián Tárnok ◽  
Sándor Borbély ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Protein Kinase ◽  
Dendritic Spines ◽  
Morphological Changes ◽  
Long Term Potentiation ◽  
Memory Formation ◽  
Protein Kinase D

Actin turnover in dendritic spines influences spine development, morphology, and plasticity, with functional consequences on learning and memory formation. In nonneuronal cells, protein kinase D (PKD) has an important role in stabilizing F-actin via multiple molecular pathways. Using in vitro models of neuronal plasticity, such as glycine-induced chemical long-term potentiation (LTP), known to evoke synaptic plasticity, or long-term depolarization block by KCl, leading to homeostatic morphological changes, we show that actin stabilization needed for the enlargement of dendritic spines is dependent on PKD activity. Consequently, impaired PKD functions attenuate activity-dependent changes in hippocampal dendritic spines, including LTP formation, cause morphological alterations in vivo, and have deleterious consequences on spatial memory formation. We thus provide compelling evidence that PKD controls synaptic plasticity and learning by regulating actin stability in dendritic spines.

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