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Learning of Precise Spike Times with Membrane Potential Dependent Synaptic Plasticity  [PDF]
Christian Albers,Maren Westkott,Klaus Pawelzik
Quantitative Biology , 2014,
Abstract: Precise spatio-temporal patterns of neuronal action potentials underly e.g. sensory representations and control of muscle activities. However, it is not known how the synaptic efficacies in the neuronal networks of the brain adapt such that they can reliably generate spikes at specific points in time. Existing activity-dependent plasticity rules like Spike-Timing-Dependent Plasticity are agnostic to the goal of learning spike times. On the other hand, the existing formal and supervised learning algorithms perform a temporally precise comparison of projected activity with the target, but there is no known biologically plausible implementation of this comparison. Here, we propose a simple and local unsupervised synaptic plasticity mechanism that is derived from the requirement of a balanced membrane potential. Since the relevant signal for synaptic change is the postsynaptic voltage rather than spike times, we call the plasticity rule Membrane Potential Dependent Plasticity (MPDP). Combining our plasticity mechanism with spike after-hyperpolarization causes a sensitivity of synaptic change to pre- and postsynaptic spike times which can reproduce Hebbian spike timing dependent plasticity for inhibitory synapses as was found in experiments. In addition, the sensitivity of MPDP to the time course of the voltage when generating a spike allows MPDP to distinguish between weak (spurious) and strong (teacher) spikes, which therefore provides a neuronal basis for the comparison of actual and target activity. For spatio-temporal input spike patterns our conceptually simple plasticity rule achieves a surprisingly high storage capacity for spike associations. The sensitivity of the MPDP to the subthreshold membrane potential during training allows robust memory retrieval after learning even in the presence of activity corrupted by noise.
The role of AMPA receptors in postsynaptic mechanisms of synaptic plasticity  [PDF]
Thomas E. Chater,Yukiko Goda
Frontiers in Cellular Neuroscience , 2014, DOI: 10.3389/fncel.2014.00401
Abstract: In the mammalian central nervous system, excitatory glutamatergic synapses harness neurotransmission that is mediated by ion flow through α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs). AMPARs, which are enriched in the postsynaptic membrane on dendritic spines, are highly dynamic, and shuttle in and out of synapses in an activity-dependent manner. Changes in their number, subunit composition, phosphorylation state, and accessory proteins can all regulate AMPARs and thus modify synaptic strength and support cellular forms of learning. Furthermore, dysregulation of AMPAR plasticity has been implicated in various pathological states and has important consequences for mental health. Here we focus on the mechanisms that control AMPAR plasticity, drawing particularly from the extensive studies on hippocampal synapses, and highlight recent advances in the field along with considerations for future directions.
Synaptic Plasticity with Discrete state synapses  [PDF]
H. D. Abarbanel,S. S. Talathi,L. Gibb,M. Rabinovich
Quantitative Biology , 2005, DOI: 10.1103/PhysRevE.72.031914
Abstract: Experimental observations on synaptic plasticity at individual glutamatergic synapses from the CA3 Shaffer collateral pathway onto CA1 pyramidal cells in the hippocampus suggest that the transitions in synaptic strength occur among discrete levels at individual synapses (~\cite{Peter} and S. S.-H. Wang, unpublished data used with the authors' permission). This happens for both long term potentiation (LTP) and long term depression (LTD) induction protocols. O'Connor, Wittenberg, and Wang have argued that three states would account for their observations on individual synapses in the CA3-CA1 pathway. We develop a quantitative model of this three state system with transitions among the states determined by a competition between kinases and phosphatases shown by O'Connor et al. to be determinant of LTP and LTD, respectively. Specific predictions for various plasticity protocols are given by coupling this description of discrete synaptic AMPA conductance changes to a model of postsynaptic membrane potential and associated intracellular calcium fluxes to yield the transition rates among the states. We then present various LTP and LTD induction protocols to the model system and report the resulting whole cell changes in AMPA conductance. We also examine the effect of our discrete state synaptic plasticity model on the synchronization of realistic oscillating neurons. We show that one-to-one synchronization is enhanced by the plasticity we discuss here and the presynaptic and postsynaptic oscillations are in phase. Synaptic strength saturates naturally in this model and does not require artificial upper or lower cutoffs, in contrast to earlier models of plasticity.
Astrocytes: orchestrating synaptic plasticity?  [PDF]
Maurizio De Pittà,Nicolas Brunel,Andrea Volterra
Quantitative Biology , 2015, DOI: 10.1016/j.neuroscience.2015.04.001
Abstract: Synaptic plasticity is the capacity of a preexisting connection between two neurons to change in strength as a function of neural activity. Because synaptic plasticity is the major candidate mechanism for learning and memory, the elucidation of its constituting mechanisms is of crucial importance in many aspects of normal and pathological brain function. In particular, a prominent aspect that remains debated is how the plasticity mechanisms, that encompass a broad spectrum of temporal and spatial scales, come to play together in a concerted fashion. Here we review and discuss evidence that pinpoints to a possible non-neuronal, glial candidate for such orchestration: the regulation of synaptic plasticity by astrocytes.
Imaging synaptic plasticity
Zahid Padamsey, Nigel J Emptage
Molecular Brain , 2011, DOI: 10.1186/1756-6606-4-36
Abstract: Traditionally, electrophysiological recordings and biochemical assays have been used to investigate long-term changes in synaptic efficacy following the electrical, pharmacological, or genetic manipulation of synaptic function. These methodologies limit either the spatial or temporal resolution with which biological processes can be observed and manipulated. For example, the electrophysiological characterization of long-term potentiation (LTP), as reported by increases in the amplitude of evoked postsynaptic potentials, often represents a collective change in transmission efficacy across a population of synapses rather than a direct characterization of plasticity at single sites. Moreover, the use of molecular and pharmacological techniques, although useful in elucidating the role of biochemical pathways in the induction and expression of plasticity, reveal little of the spatiotemporal dynamics of cellular signalling that follow synaptic stimulation. Such dynamics, however, are important in understanding how synaptic processing is altered across space and time following the induction of LTP.In the past decade, advances in optical imaging, combined with the use and development of fluorescent biosensors, have circumvented the problems associated with traditional experimental techniques by offering unparalleled spatiotemporal resolution of molecular events at synapses. Here, we review the use of optical imaging in recent studies of synaptic plasticity in the hippocampus, with a particular focus on how such techniques have been used to assess the 1) presynaptic and 2) postsynaptic expression of LTP, and 3) to examine the spatiotemporal dynamics of plasticity-related signalling.Changes in synaptic efficacy are supported by changes at either pre- or post- synaptic sites [1]. Within the hippocampus, the locus of LTP expression has been a point of contention for many years, in part, due to the difficulties in dissociating the pre- and post- synaptic components of plasticity
A Ca2+-based computational model for NDMA receptor-dependent synaptic plasticity at individual post-synaptic spines in the hippocampus  [PDF]
Owen J. L. Rackham,Krasimira Tsaneva-Atanasova,Ayalvadi Ganesh,Jack R. Mellor
Frontiers in Synaptic Neuroscience , 2010, DOI: 10.3389/fnsyn.2010.00031
Abstract: Associative synaptic plasticity is synapse specific and requires coincident activity in pre-synaptic and post-synaptic neurons to activate NMDA receptors (NMDARs). The resultant Ca2+ influx is the critical trigger for the induction of synaptic plasticity. Given its centrality for the induction of synaptic plasticity, a model for NMDAR activation incorporating the timing of pre-synaptic glutamate release and post-synaptic depolarization by back-propagating action potentials could potentially predict the pre- and post-synaptic spike patterns required to induce synaptic plasticity. We have developed such a model by incorporating currently available data on the timecourse and amplitude of the post-synaptic membrane potential within individual spines. We couple this with data on the kinetics of synaptic NMDARs and then use the model to predict the continuous spine [Ca2+] in response to regular or irregular pre- and post-synaptic spike patterns. We then incorporate experimental data from synaptic plasticity induction protocols by regular activity patterns to couple the predicted local peak [Ca2+] to changes in synaptic strength. We find that our model accurately describes [Ca2+] in dendritic spines resulting from NMDAR activation during pre-synaptic and post-synaptic activity when compared to previous experimental observations. The model also replicates the experimentally determined plasticity outcome of regular and irregular spike patterns when applied to a single synapse. This model could therefore be used to predict the induction of synaptic plasticity under a variety of experimental conditions and spike patterns.
Synaptic Neurotransmission Depression in Ventral Tegmental Dopamine Neurons and Cannabinoid-Associated Addictive Learning  [PDF]
Zhiqiang Liu,Jing Han,Lintao Jia,Jean-Christian Maillet,Guang Bai,Lin Xu,Zhengping Jia,Qiaohua Zheng,Wandong Zhang,Robert Monette,Zul Merali,Zhou Zhu,Wei Wang,Wei Ren,Xia Zhang
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0015634
Abstract: Drug addiction is an association of compulsive drug use with long-term associative learning/memory. Multiple forms of learning/memory are primarily subserved by activity- or experience-dependent synaptic long-term potentiation (LTP) and long-term depression (LTD). Recent studies suggest LTP expression in locally activated glutamate synapses onto dopamine neurons (local Glu-DA synapses) of the midbrain ventral tegmental area (VTA) following a single or chronic exposure to many drugs of abuse, whereas a single exposure to cannabinoid did not significantly affect synaptic plasticity at these synapses. It is unknown whether chronic exposure of cannabis (marijuana or cannabinoids), the most commonly used illicit drug worldwide, induce LTP or LTD at these synapses. More importantly, whether such alterations in VTA synaptic plasticity causatively contribute to drug addictive behavior has not previously been addressed. Here we show in rats that chronic cannabinoid exposure activates VTA cannabinoid CB1 receptors to induce transient neurotransmission depression at VTA local Glu-DA synapses through activation of NMDA receptors and subsequent endocytosis of AMPA receptor GluR2 subunits. A GluR2-derived peptide blocks cannabinoid-induced VTA synaptic depression and conditioned place preference, i.e., learning to associate drug exposure with environmental cues. These data not only provide the first evidence, to our knowledge, that NMDA receptor-dependent synaptic depression at VTA dopamine circuitry requires GluR2 endocytosis, but also suggest an essential contribution of such synaptic depression to cannabinoid-associated addictive learning, in addition to pointing to novel pharmacological strategies for the treatment of cannabis addiction.
Actin- and Dynamin-Dependent Maturation of Bulk Endocytosis Restores Neurotransmission following Synaptic Depletion  [PDF]
Tam H. Nguyen, Guillaume Maucort, Robert K. P. Sullivan, Mitja Schenning, Nickolas A. Lavidis, Adam McCluskey, Phillip J. Robinson, Frederic A. Meunier
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0036913
Abstract: Bulk endocytosis contributes to the maintenance of neurotransmission at the amphibian neuromuscular junction by regenerating synaptic vesicles. How nerve terminals internalize adequate portions of the presynaptic membrane when bulk endocytosis is initiated before the end of a sustained stimulation is unknown. A maturation process, occurring at the end of the stimulation, is hypothesised to precisely restore the pools of synaptic vesicles. Using confocal time-lapse microscopy of FM1-43-labeled nerve terminals at the amphibian neuromuscular junction, we confirm that bulk endocytosis is initiated during a sustained tetanic stimulation and reveal that shortly after the end of the stimulation, nerve terminals undergo a maturation process. This includes a transient bulging of the plasma membrane, followed by the development of large intraterminal FM1-43-positive donut-like structures comprising large bulk membrane cisternae surrounded by recycling vesicles. The degree of bulging increased with stimulation frequency and the plasmalemma surface retrieved following the transient bulging correlated with the surface membrane internalized in bulk cisternae and recycling vesicles. Dyngo-4a, a potent dynamin inhibitor, did not block the initiation, but prevented the maturation of bulk endocytosis. In contrast, cytochalasin D, an inhibitor of actin polymerization, hindered both the initiation and maturation processes. Both inhibitors hampered the functional recovery of neurotransmission after synaptic depletion. Our data confirm that initiation of bulk endocytosis occurs during stimulation and demonstrates that a delayed maturation process controlled by actin and dynamin underpins the coupling between exocytosis and bulk endocytosis.
The Remarkable Mechanism of Prostaglandin E2 on Synaptic Plasticity
Yukio Akaneya
Gene Regulation and Systems Biology , 2007,
Abstract: Prostanoids have a broad spectrum of biological activities in a variety of organs including the brain. However, their effects on synaptic plasticity in the brain, which have been recently revealed, are ambiguous in comparison to those in the other organs. Prostaglandin E2 (PGE) is a prostanoid produced from arachidonic acid in the cellular membrane, and knowledge about its functions is increasing. Recently, a novel function of PGE2 in the brain has shed light on aspects of synaptic plasticity such as long-term potentiation (LTP). More recently, we have proposed a hypothesis for the mechanisms of this PGE2-related form of synaptic plasticity in the visual cortex. This involves the dynamics of two subtypes of PGE2 receptors that have opposing functions in intracellular signal transduction. Consequently, mechanisms that increase the level of cyclic AMP in the cytosol may explain for the mechanisms of LTP in the visual cortex. The current notion of bidirectional traf cking of PGE2 receptors under this hypothesis is reminiscent of the “silent synapse” mechanism of LTP on the traf cking of the AMPA receptors between the membrane and cytosol. Moreover, we propose the hypothesis that PGE2 acts as a “post-to-postsynaptic messenger” for the induction of LTP in the visual cortex. This review describes a complex mode of action of PGE2 receptors in synaptic plasticity in the brain.
A link between ECM plasticity and synaptic morphological evolution  [PDF]
S. Kanani,I. Robbins,T. Biben,N. Olivi-Tran
Physics , 2007,
Abstract: We made a link between Extra Cellular Matrix (ECM) plasticity and the morphologi cal changes in synapses after synaptic excitation. A recent study by Zhang et al \cite{zhang} showed tha t transmembrane voltage causes movement of the cell membrane. Here we will study the relation between th e mechanical properties of collagen which is the major component of the ECM and synaptic morphological c hanges in relation with the theory of DO Hebb \cite{hebb}
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