scholarly journals Synaptic plasticity, neural circuits, and the emerging role of altered short-term information processing in schizophrenia

2014 ◽  
Vol 6 ◽  
Author(s):  
Gregg W. Crabtree ◽  
Joseph A. Gogos
Keyword(s):  
Information Processing ◽  
Synaptic Plasticity ◽  
Neural Circuits ◽  
Short Term

Synapsin Regulates Basal Synaptic Strength, Synaptic Depression, and Serotonin-Induced Facilitation of Sensorimotor Synapses in Aplysia

2007 ◽  
Vol 98 (6) ◽  
pp. 3568-3580 ◽  
Author(s):  
Diasinou Fioravante ◽  
Rong-Yu Liu ◽  
Anne K. Netek ◽  
Leonard J. Cleary ◽  
John H. Byrne
Keyword(s):  
Synaptic Plasticity ◽  
Synaptic Vesicle ◽  
Transmitter Release ◽  
Computational Analysis ◽  
Spontaneous Recovery ◽  
Synaptic Strength ◽  
Short Term ◽  
Homosynaptic Depression ◽  
Heterosynaptic Plasticity

Synapsin is a synaptic vesicle-associated protein implicated in the regulation of vesicle trafficking and transmitter release, but its role in heterosynaptic plasticity remains elusive. Moreover, contradictory results have obscured the contribution of synapsin to homosynaptic plasticity. We previously reported that the neuromodulator serotonin (5-HT) led to the phosphorylation and redistribution of Aplysia synapsin, suggesting that synapsin may be a good candidate for the regulation of vesicle mobilization underlying the short-term synaptic plasticity induced by 5-HT. This study examined the role of synapsin in homosynaptic and heterosynaptic plasticity. Overexpression of synapsin reduced basal transmission and enhanced homosynaptic depression. Although synapsin did not affect spontaneous recovery from depression, it potentiated 5-HT–induced dedepression. Computational analysis showed that the effects of synapsin on plasticity could be adequately simulated by altering the rate of Ca2+-dependent vesicle mobilization, supporting the involvement of synapsin not only in homosynaptic but also in heterosynaptic forms of plasticity by regulating vesicle mobilization.

Long-term depression of Aplysia sensorimotor synapses in cell culture: inductive role of a rise in postsynaptic calcium

1996 ◽  
Vol 76 (3) ◽  
pp. 2111-2114 ◽  
Author(s):  
X. Y. Lin ◽  
D. L. Glanzman
Keyword(s):  
Cell Culture ◽  
Synaptic Plasticity ◽  
Sensory Neurons ◽  
Tetraacetic Acid ◽  
Short Term ◽  
Long Term Depression ◽  
Central Synapses ◽  
Postsynaptic Calcium

1. Activation of sensory neurons at 2 Hz for 15 min induces long-term depression (LTD) of isolated Aplysia sensorimotor synapses in cell culture. 2. Prior infusion of the Ca2+ chelator 1,2-bis-(2-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA) into the postsynaptic motor neuron blocks the induction of LTD, but not short-term synaptic depression. 3. Invertebrate central synapses possess the capacity for LTD. This form of long-term synaptic plasticity may play an important role in learning in Aplysia.

scholarly journals Role of the calcium-binding protein parvalbumin in short-term synaptic plasticity

2000 ◽  
Vol 97 (24) ◽  
pp. 13372-13377 ◽  
Author(s):  
O. Caillard ◽  
H. Moreno ◽  
B. Schwaller ◽  
I. Llano ◽  
M. R. Celio ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Calcium Binding ◽  
Binding Protein ◽  
Calcium Binding Protein ◽  
Short Term

scholarly journals Dynamic modulation of short-term synaptic plasticity in the auditory cortex: The role of norepinephrine

2011 ◽  
Vol 271 (1-2) ◽  
pp. 26-36 ◽  
Author(s):  
Humberto Salgado ◽  
Francisco García-Oscos ◽  
Lu Dinh ◽  
Marco Atzori
Keyword(s):  
Synaptic Plasticity ◽  
Auditory Cortex ◽  
Short Term ◽  
Dynamic Modulation

Role of Ca2+ channels in short-term synaptic plasticity

2007 ◽  
Vol 17 (3) ◽  
pp. 352-359 ◽  
Author(s):  
Jianhua Xu ◽  
Liming He ◽  
Ling-Gang Wu
Keyword(s):  
Synaptic Plasticity ◽  
Short Term ◽  
Ca2 Channels

scholarly journals Expression and role of Galectin-3 in the postnatal development of the cerebellum

2018 ◽  
Author(s):  
Inés González-Calvo ◽  
Fekrije Selimi
Keyword(s):  
Synaptic Plasticity ◽  
Immune System ◽  
Purkinje Cell ◽  
Axon Guidance ◽  
Neuronal Migration ◽  
Neural Circuits ◽  
Related Protein ◽  
Galectin 3 ◽  
The Brain

AbstractMany proteins initially identified in the immune system play roles in neurogenesis, neuronal migration, axon guidance, synaptic plasticity and other processes related to the formation and refinement of neural circuits. Although the function of the immune-related protein Galectin-3 (LGALS3) has been extensively studied in the regulation of inflammation, cancer and microglia activation, little is known about its role in the development of the brain. In this study, we identified that LGALS3 is expressed in the developing postnatal cerebellum. More precisely, LGALS3 is expressed by cells in meninges and in the choroid plexus, and in subpopulations of astrocytes and of microglial cells in the cerebellar cortex. Analysis of Lgals3 knockout mice showed that Lgals3 is dispensable for the development of cerebellar cytoarchitecture and Purkinje cell excitatory synaptogenesis in the mouse.

scholarly journals Learning to Discriminate Through Long-Term Changes of Dynamical Synaptic Transmission

2009 ◽  
Vol 21 (12) ◽  
pp. 3408-3428 ◽  
Author(s):  
Christian Leibold ◽  
Michael H. K. Bendels
Keyword(s):  
Synaptic Plasticity ◽  
Learning Rule ◽  
Recurrent Network ◽  
Short Term ◽  
Input Space ◽  
Capacity Limit ◽  
Classical Receptive Field ◽  
Synaptic Changes

Short-term synaptic plasticity is modulated by long-term synaptic changes. There is, however, no general agreement on the computational role of this interaction. Here, we derive a learning rule for the release probability and the maximal synaptic conductance in a circuit model with combined recurrent and feedforward connections that allows learning to discriminate among natural inputs. Short-term synaptic plasticity thereby provides a nonlinear expansion of the input space of a linear classifier, whereas the random recurrent network serves to decorrelate the expanded input space. Computer simulations reveal that the twofold increase in the number of input dimensions through short-term synaptic plasticity improves the performance of a standard perceptron up to 100%. The distributions of release probabilities and maximal synaptic conductances at the capacity limit strongly depend on the balance between excitation and inhibition. The model also suggests a new computational interpretation of spikes evoked by stimuli outside the classical receptive field. These neuronal activities may reflect decorrelation of the expanded stimulus space by intracortical synaptic connections.

scholarly journals Estimating short-term synaptic plasticity from pre- and postsynaptic spiking

2017 ◽  
Author(s):  
Abed Ghanbari ◽  
Aleksey Malyshev ◽  
Maxim Volgushev ◽  
Ian H. Stevenson
Keyword(s):  
Information Processing ◽  
Synaptic Plasticity ◽  
Intracellular Recordings ◽  
Coupling Term ◽  
Short Term ◽  
Short Term Plasticity ◽  
Postsynaptic Spike ◽  
Model Based ◽  
Different Types ◽  
Synaptic Dynamics

AbstractShort-term synaptic plasticity (STP) critically affects the processing of information in neuronal circuits by reversibly changing the effective strength of connections between neurons on time scales from milliseconds to a few seconds. STP is traditionally studied using intracellular recordings of postsynaptic potentials or currents evoked by presynaptic spikes. However, STP also affects the statistics of postsynaptic spikes. Here we present two model-based approaches for estimating synaptic weights and short-term plasticity from pre- and postsynaptic spike observations alone. We extend a generalized linear model (GLM) that predicts postsynaptic spiking as a function of the observed pre- and postsynaptic spikes and allow the connection strength (coupling term in the GLM) to vary as a function of time based on the history of presynaptic spikes. Our first model assumes that STP follows a Tsodyks-Markram description of vesicle depletion and recovery. In a second model, we introduce a functional description of STP where we estimate the coupling term as a biophysically unrestrained function of the presynaptic inter-spike intervals. To validate the models, we test the accuracy of STP estimation using the spiking of pre- and postsynaptic neurons with known synaptic dynamics. We first test our models using the responses of layer 2/3 pyramidal neurons to simulated presynaptic input with different types of STP, and then use simulated spike trains to examine the effects of spike-frequency adaptation, stochastic vesicle release, spike sorting errors, and common input. We find that, using only spike observations, both model-based methods can accurately reconstruct the time-varying synaptic weights of presynaptic inputs for different types of STP. Our models also capture the differences in postsynaptic spike responses to presynaptic spikes following short vs long inter-spike intervals, similar to results reported for thalamocortical connections. These models may thus be useful tools for characterizing short-term plasticity from multi-electrode spike recordings in vivo.Author SummaryInformation processing in the nervous system critically depends on dynamic changes in the strength of connections between neurons. Short-term synaptic plasticity (STP), changes that occur on timescales from milliseconds to a few seconds, is thought to play a role in tasks such as speech recognition, motion detection, and working memory. Although intracellular recordings in slices of neural tissue have identified synaptic mechanisms of STP and have demonstrated its potential role in information processing, studying STP in intact animals, especially during behavior, is experimentally difficult. Unlike intracellular recordings, extracellular spiking of hundreds of neurons simultaneously can be recorded even in behaving animals. Here we developed two models that allow estimation of STP from extracellular spike recordings. We validate these models using results from in vitro experiments which simulate a realistic synaptic input from a population of presynaptic neurons with defined STP rules. Our results show that both new models can accurately recover the synaptic dynamics underlying spiking. These new methods will allow us to study STP using extracellular recordings, and therefore on a much larger scale than previously possible in behaving animals.

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