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 Learning complex temporal patterns with resource-dependent spike timing-dependent plasticity

2012 ◽  
Vol 108 (2) ◽  
pp. 551-566 ◽  
Author(s):  
Jason F. Hunzinger ◽  
Victor H. Chan ◽  
Robert C. Froemke
Keyword(s):  
Long Term Potentiation ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Rate Dependent ◽  
Temporal Relationships ◽  
Term Potentiation ◽  
Functional Mechanisms

Studies of spike timing-dependent plasticity (STDP) have revealed that long-term changes in the strength of a synapse may be modulated substantially by temporal relationships between multiple presynaptic and postsynaptic spikes. Whereas long-term potentiation (LTP) and long-term depression (LTD) of synaptic strength have been modeled as distinct or separate functional mechanisms, here, we propose a new shared resource model. A functional consequence of our model is fast, stable, and diverse unsupervised learning of temporal multispike patterns with a biologically consistent spiking neural network. Due to interdependencies between LTP and LTD, dendritic delays, and proactive homeostatic aspects of the model, neurons are equipped to learn to decode temporally coded information within spike bursts. Moreover, neurons learn spike timing with few exposures in substantial noise and jitter. Surprisingly, despite having only one parameter, the model also accurately predicts in vitro observations of STDP in more complex multispike trains, as well as rate-dependent effects. We discuss candidate commonalities in natural long-term plasticity mechanisms.

Spike Timing-Dependent Plasticity: From Synapse to Perception

2006 ◽  
Vol 86 (3) ◽  
pp. 1033-1048 ◽  
Author(s):  
Yang Dan ◽  
Mu-Ming Poo
Keyword(s):  
Neuronal Excitability ◽  
Human Perception ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Functional Changes

Information in the nervous system may be carried by both the rate and timing of neuronal spikes. Recent findings of spike timing-dependent plasticity (STDP) have fueled the interest in the potential roles of spike timing in processing and storage of information in neural circuits. Induction of long-term potentiation (LTP) and long-term depression (LTD) in a variety of in vitro and in vivo systems has been shown to depend on the temporal order of pre- and postsynaptic spiking. Spike timing-dependent modification of neuronal excitability and dendritic integration was also observed. Such STDP at the synaptic and cellular level is likely to play important roles in activity-induced functional changes in neuronal receptive fields and human perception.

scholarly journals Long-term population spike-timing-dependent plasticity promotes synaptic tagging but not cross-tagging in rat hippocampal area CA1

2019 ◽  
Vol 116 (12) ◽  
pp. 5737-5746 ◽  
Author(s):  
Karen Ka Lam Pang ◽  
Mahima Sharma ◽  
Kumar Krishna-K. ◽  
Thomas Behnisch ◽  
Sreedharan Sajikumar
Keyword(s):  
Synaptic Plasticity ◽  
Long Term Potentiation ◽  
Neuronal Population ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Adult Rat ◽  
Term Potentiation ◽  
Hippocampal Ca3

In spike-timing-dependent plasticity (STDP), the direction and degree of synaptic modification are determined by the coherence of pre- and postsynaptic activities within a neuron. However, in the adult rat hippocampus, it remains unclear whether STDP-like mechanisms in a neuronal population induce synaptic potentiation of a long duration. Thus, we asked whether the magnitude and maintenance of synaptic plasticity in a population of CA1 neurons differ as a function of the temporal order and interval between pre- and postsynaptic activities. Modulation of the relative timing of Schaffer collateral fibers (presynaptic component) and CA1 axons (postsynaptic component) stimulations resulted in an asymmetric population STDP (pSTDP). The resulting potentiation in response to 20 pairings at 1 Hz was largest in magnitude and most persistent (4 h) when presynaptic activity coincided with or preceded postsynaptic activity. Interestingly, when postsynaptic activation preceded presynaptic stimulation by 20 ms, an immediate increase in field excitatory postsynaptic potentials was observed, but it eventually transformed into a synaptic depression. Furthermore, pSTDP engaged in selective forms of late-associative activity: It facilitated the maintenance of tetanization-induced early long-term potentiation (LTP) in neighboring synapses but not early long-term depression, reflecting possible mechanistic differences with classical tetanization-induced LTP. The data demonstrate that a pairing of pre- and postsynaptic activities in a neuronal population can greatly reduce the required number of synaptic plasticity-evoking events and induce a potentiation of a degree and duration similar to that with repeated tetanization. Thus, pSTDP determines synaptic efficacy in the hippocampal CA3–CA1 circuit and could bias the CA1 neuronal population toward potentiation in future events.

Caffeine-Mediated Presynaptic Long-Term Potentiation in Hippocampal CA1 Pyramidal Neurons

2003 ◽  
Vol 89 (6) ◽  
pp. 3029-3038 ◽  
Author(s):  
Eduardo D. Martín ◽  
Washington Buño
Keyword(s):  
Nmda Receptors ◽  
Glutamate Release ◽  
Ryanodine Receptors ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Cellular Mechanisms ◽  
Pipette Solution ◽  
Term Potentiation

We report a new form of long-term potentiation (LTP) in Schaffer collateral (SC)-CA1 pyramidal neuron synapses that originates presynaptically and does not require N-methyl-d-aspartate (NMDA) receptor activation nor increases in postsynaptic-free Ca2+. Using rat hippocampal slices, application of a brief “pulse” of caffeine in the bath evoked a nondecremental LTP (CAFLTP) of SC excitatory postsynaptic currents. An increased probability of transmitter release paralleled the CAFLTP, suggesting that it originated presynaptically. The P1 adenosine receptor antagonist 8-cyclopentyltheophylline and the P2 purinoreceptor antagonists suramin and piridoxal-5′-phosphate-azophenyl 2′,4′-disulphonate blocked the CAFLTP. Inhibition of Ca2+ release from caffeine/ryanodine stores by bath-applied ryanodine inhibited the CAFLTP, but ryanodine in the pipette solution was ineffective, suggesting a presynaptic effect of ryanodine. Previous induction of the “classical” LTP did not prevent the CAFLTP, suggesting that the LTP and the CAFLTP have different underlying cellular mechanisms. The CAFLTP is insensitive to the block of NMDA receptors by 2-amino-5-phosphonopentanoic acid and to Ca2+ chelation with intracellular 1,2-bis (2-aminophenoxy) ethane- N,N,N′ ,N′-tetraacetic acid, indicating that neither postsynaptic NMDA receptors nor increases in cytosolic-free Ca2+ participate in the CAFLTP. We conclude that the CAFLTP requires the interaction of caffeine with presynaptic P1, P2 purinoreceptors, and ryanodine receptors and is caused by an increased probability of glutamate release at SC terminals.

scholarly journals Effect of Interpopulation Spike-Timing-Dependent Plasticity on Synchronized Rhythms in Neuronal Networks with Inhibitory and Excitatory Populations

2019 ◽  
Author(s):  
Sang-Yoon Kim ◽  
Woochang Lim
Keyword(s):  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Term Potentiation ◽  
Wide Range ◽  
Raster Plot ◽  
Average Fraction

We consider a two-population network consisting of both inhibitory (I) interneurons and excitatory (E) pyramidal cells. This I-E neuronal network has adaptive dynamic I to E and E to I interpopulation synaptic strengths, governed by interpopulation spike-timing-dependent plasticity (STDP). In previous works without STDPs, fast sparsely synchronized rhythms, related to diverse cognitive functions, were found to appear in a range of noise intensity D for static synaptic strengths. Here, by varying D, we investigate the effect of interpopulation STDPs on fast sparsely synchronized rhythms that emerge in both the I- and the E-populations. Depending on values of D, long-term potentiation (LTP) and long-term depression (LTD) for population-averaged values of saturated interpopulation synaptic strengths are found to occur. Then, the degree of fast sparse synchronization varies due to effects of LTP and LTD. In a broad region of intermediate D, the degree of good synchronization (with higher synchronization degree) becomes decreased, while in a region of large D, the degree of bad synchronization (with lower synchronization degree) gets increased. Consequently, in each I- or E-population, the synchronization degree becomes nearly the same in a wide range of D (including both the intermediate and the large D regions). This kind of “equalization effect” is found to occur via cooperative interplay between the average occupation and pacing degrees of spikes (i.e., the average fraction of firing neurons and the average degree of phase coherence between spikes in each synchronized stripe of spikes in the raster plot of spikes) in fast sparsely synchronized rhythms. Finally, emergences of LTP and LTD of interpopulation synaptic strengths (leading to occurrence of equalization effect) are intensively investigated via a microscopic method based on the distributions of time delays between the pre- and the post-synaptic spike times.PACS numbers87.19.lw, 87.19.lm, 87.19.lc

scholarly journals Muscarinic modulation of spike-timing dependent plasticity at recurrent layer 2/3 synapses in mouse auditory cortex

2019 ◽  
Author(s):  
Deepti Rao ◽  
Megan B. Kratz ◽  
Paul B. Manis
Keyword(s):  
Auditory Cortex ◽  
Pyramidal Neurons ◽  
Long Term Potentiation ◽  
Spike Timing ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Receptor Modulation ◽  
Intracortical Circuits ◽  
Layer 2

AbstractCholinergic systems contribute to the refinement of auditory cortical receptive fields by activating muscarinic acetylcholine receptors (mAChRs). However, the specific cellular and synaptic mechanisms underlying acetylcholine’s effects on cortical circuits are not fully understood. In this study, we investigate the effects of muscarinic receptor modulation on spike-timing dependent plasticity (STDP) at synapses onto layer 2/3 pyramidal neurons in mouse auditory cortex (AC). Synapses onto layer 2/3 pyramidal neurons exhibit a STDP rule for pairing of postsynaptic spike bursts with single presynaptic stimuli. Pre-before-post pairing at +10 ms results in a timing-dependent long-term potentiation (tLTP), whereas pre-before-post pairing at +50 ms intervals, and post-before-pre pairing at -10 to -20 ms produce a timing-dependent long-term depression. We also characterize how mAChR activation affects plasticity at these synapses, focusing on the induction of tLTP. During pre-before-post pairing at +10 ms, mAChR activation by either carbachol or oxotremorine-M suppresses tLTP. mAChR activation also reduces the NMDA-receptor dependent synaptically evoked increase in calcium in dendrites, apparently without affecting presynaptic transmitter release. Pharmacological experiments suggest that M1 and M3 receptors are not involved in the mAChR-mediated suppression of tLTP. Taken together, these results suggest activating mAChRs in layer 2/3 intracortical circuits can modify the circuit dynamics of AC by depressing tLTP mediated by NMDA receptors, and depressing calcium influx at excitatory synapses onto layer 2/3 pyramidal cells.

scholarly journals Early Postnatal Plasticity in Neocortex of Fmr1 Knockout Mice

2006 ◽  
Vol 96 (4) ◽  
pp. 1734-1745 ◽  
Author(s):  
Niraj S. Desai ◽  
Tanya M. Casimiro ◽  
Stephen M. Gruber ◽  
Peter W. Vanderklish
Keyword(s):  
Knockout Mice ◽  
Developmental Plasticity ◽  
Fragile X ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Spike Timing ◽  
Term Potentiation ◽  
Spine Abnormalities ◽  
Intrinsic Plasticity

Fragile X syndrome is produced by a defect in a single X-linked gene, called Fmr1, and is characterized by abnormal dendritic spine morphologies with spines that are longer and thinner in neocortex than those from age-matched controls. Studies using Fmr1 knockout mice indicate that spine abnormalities are especially pronounced in the first month of life, suggesting that altered developmental plasticity underlies some of the behavioral phenotypes associated with the syndrome. To address this issue, we used intracellular recordings in neocortical slices from early postnatal mice to examine the effects of Fmr1 disruption on two forms of plasticity active during development. One of these, long-term potentiation of intrinsic excitability, is intrinsic in expression and requires mGluR5 activation. The other, spike timing-dependent plasticity, is synaptic in expression and requires N-methyl-d-aspartate receptor activation. While intrinsic plasticity was normal in the knockout mice, synaptic plasticity was altered in an unusual and striking way: long-term depression was robust but long-term potentiation was entirely absent. These findings underscore the ideas that Fmr1 has highly selective effects on plasticity and that abnormal postnatal development is an important component of the disorder.

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