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Eric R. Kandel - One of the best experts on this subject based on the ideXlab platform.
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microrna 22 gates long term Heterosynaptic Plasticity in aplysia through presynaptic regulation of cpeb and downstream targets
Cell Reports, 2015Co-Authors: Ferdinando Fiumara, Priyamvada Rajasethupathy, Igor Antonov, Stylianos Kosmidis, Wayne S Sossin, Eric R. KandelAbstract:The maintenance phase of memory-related long-term facilitation (LTF) of synapses between sensory and motor neurons of the gill-withdrawal reflex of Aplysia depends on a serotonin (5-HT)-triggered presynaptic upregulation of CPEB, a functional prion that regulates local protein synthesis at the synapse. The mechanisms whereby serotonin regulates CPEB levels in presynaptic sensory neurons are not known. Here, we describe a sensory neuron-specific microRNA 22 (miR-22) that has multiple binding sites on the mRNA of CPEB and inhibits it in the basal state. Serotonin triggers MAPK/Erk-dependent downregulation of miR-22, thereby upregulating the expression of CPEB, which in turn regulates, through functional CPE elements, the presynaptic expression of atypical PKC (aPKC), another candidate regulator of memory maintenance. Our findings support a model in which the neurotransmitter-triggered downregulation of miR-22 coordinates the regulation of genes contributing synergistically to the long-term maintenance of memory-related synaptic Plasticity.
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increased attention to spatial context increases both place field stability and spatial memory
Neuron, 2004Co-Authors: Clifford Kentros, Robert D. Hawkins, Eric R. Kandel, Naveen T Agnihotri, Samantha StreaterAbstract:Abstract The hippocampal formation is critical for the acquisition and consolidation of memories. When recorded in freely moving animals, hippocampal pyramidal neurons fire in a location-specific manner: they are "place" cells, comprising a hippocampal representation of the animal's environment. To explore the relationship between place cells and spatial memory, we recorded from mice in several behavioral contexts. We found that long-term stability of place cell firing fields correlates with the degree of attentional demands and that successful spatial task performance was associated with stable place fields. Furthermore, conditions that maximize place field stability greatly increase orientation to novel cues. This suggests that storage and retrieval of place cells is modulated by a top-down cognitive process resembling attention and that place cells are neural correlates of spatial memory. We propose a model whereby attention provides the requisite neuromodulatation to switch short-term homosynaptic Plasticity to long-term Heterosynaptic Plasticity, and we implicate dopamine in this process.
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Is Heterosynaptic modulation essential for stabilizing hebbian plasiticity and memory
Nature Reviews Neuroscience, 2000Co-Authors: Craig H. Bailey, Maurizio Giustetto, Yan-you Huang, Robert D. Hawkins, Eric R. KandelAbstract:In 1894, Ramón y Cajal first proposed that memory is stored as an anatomical change in the strength of neuronal connections. For the following 60 years, little evidence was recruited in support of this idea. This situation changed in the middle of the twentieth century with the development of cellular techniques for the study of synaptic connections and the emergence of new formulations of synaptic Plasticity that redefined Ramón y Cajal's idea, making it more suitable for testing. These formulations defined two categories of Plasticity, referred to as homosynaptic or Hebbian activity-dependent, and Heterosynaptic or modulatory input-dependent. Here we suggest that Hebbian mechanisms are used primarily for learning and for short-term memory but often cannot, by themselves, recruit the events required to maintain a long-term memory. In contrast, Heterosynaptic Plasticity commonly recruits long-term memory mechanisms that lead to transcription and to synaptic growth. When jointly recruited, homosynaptic mechanisms assure that learning is effectively established and Heterosynaptic mechanisms ensure that memory is maintained. Modern formulations of synaptic Plasticity have led to the definition of two broad categories — homosynaptic or Hebbian activity-dependent and Heterosynaptic or modulatory input-dependent. In homosynaptic Plasticity, the events responsible for triggering the plastic change occur at the same connection being strengthened or weakened. In Heterosynaptic Plasticity, the plastic change can occur in the absence of activity of the synapse being strengthened but, instead, as a result of a third, modulatory interneuron. Homosynaptic Hebbian Plasticity in both invertebrate and in mammalian synapses involves the covalent modification of pre-existing synaptic proteins and, when initiated by itself, it often lasts only for one or at most a few hours. In contrast, Heterosynaptic mechanisms can readily lead to plastic changes that last for one or more days and can, by themselves, recruit the cellular machinery necessary for the synthesis of new proteins and for the growth of new synapses. In invertebrate ( Aplysia ) synapses, the combination of homo- and Heterosynaptic mechanisms can result in new categories of synaptic Plasticity. For example, when recruited together, the duration of the plastic change can increase in a non-additive way. In addition, the combined mechanisms can restrict the long-term plastic change to a set of synapses smaller than either mechanism alone, thereby sharpening its synapse-specificity. A similar interaction between homosynaptic and Heterosynaptic mechanisms might occur in mammalian synapses but a rigorous demonstration is still missing. Nevertheless, the observation that the blockade of modulatory neurotransmitters prevents the generation of long-lasting changes of synaptic strength indicates that Heterosynaptic Plasticity probably also contributes to the stabilization of short-term memory in the mammalian brain. One possible functional significance of this interaction is that homosynaptic mechanisms are used by the nervous system to ensure that learning is effectively established; once learning has taken place, Heterosynaptic mechanisms ensure that a long-term memory is maintained.
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Is Heterosynaptic modulation essential for stabilizing Hebbian Plasticity and memory
Nature reviews. Neuroscience, 2000Co-Authors: Craig H. Bailey, Maurizio Giustetto, Yan-you Huang, Robert D. Hawkins, Eric R. KandelAbstract:In 1894, Ramon y Cajal first proposed that memory is stored as an anatomical change in the strength of neuronal connections. For the following 60 years, little evidence was recruited in support of this idea. This situation changed in the middle of the twentieth century with the development of cellular techniques for the study of synaptic connections and the emergence of new formulations of synaptic Plasticity that redefined Ramon y Cajal's idea, making it more suitable for testing. These formulations defined two categories of Plasticity, referred to as homosynaptic or Hebbian activity-dependent, and Heterosynaptic or modulatory input-dependent. Here we suggest that Hebbian mechanisms are used primarily for learning and for short-term memory but often cannot, by themselves, recruit the events required to maintain a long-term memory. In contrast, Heterosynaptic Plasticity commonly recruits long-term memory mechanisms that lead to transcription and to synpatic growth. When jointly recruited, homosynaptic mechanisms assure that learning is effectively established and Heterosynaptic mechanisms ensure that memory is maintained.
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Inhibitors of protein and RNA synthesis block structural changes that accompany long-term Heterosynaptic Plasticity in Aplysia
Neuron, 1992Co-Authors: Craig H. Bailey, Eric R. Kandel, P.g. Montarolo, Mary Chen, Samuel SchacherAbstract:Synaptic connections between the sensory and motor neurons of Aplysia in culture undergo long-term facilitation in response to serotonin (5-HT) and long-term depression in response to FMRFamide. These long-term functional changes are dependent on the synthesis of macromolecules during the period in which the transmitter is applied and are accompanied by structural changes. There is an increase and a decrease, respectively, in the number of sensory neuron varicosities in response to 5-HT and FMRFamide. To determine whether macromolecular synthesis is also required for the structural changes, we examined in parallel the effects of inhibitors of protein (anisomycin) or RNA (actinomycin D) synthesis on the structural and functional changes. We have found that anisomycin and actinomycin D block both the enduring alterations in varicosity number and the long-lasting changes in synaptic potential. These results indicate that macromolecular synthesis is required for expression of the long-lasting structural changes in the sensory cells and that this synthesis is correlated with the long-term functional modulation of sensorimotor synapses.
Maxim Volgushev - One of the best experts on this subject based on the ideXlab platform.
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Altered Heterosynaptic Plasticity impairs visual discrimination learning in adenosine A1 receptor knockout mice
2020Co-Authors: Renee Chasse, Alexey Y. Malyshev, R. Holly Fitch, Maxim VolgushevAbstract:Theoretical and modeling studies demonstrate that Heterosynaptic Plasticity - changes at synapses inactive during induction - facilitates fine-grained discriminative learning in Hebbian-type systems, and helps to achieve a robust ability for repetitive learning. A dearth of tools for selective manipulation has hindered experimental analysis of the proposed role of Heterosynaptic Plasticity in behavior. Here we circumvent this obstacle by testing specific predictions about changes in Heterosynaptic Plasticity, and associated behavioral consequences, following experimental manipulation of adenosine A1 receptors (A1R). We show that, compared to wild-type controls, A1R-knockout mice have impaired synaptic Plasticity in visual cortex neurons, coupled with significant deficits in visual discrimination learning. Deficits in A1R-knockouts were seen specifically during re-learning, becoming progressively more apparent with learning on sequential visual discrimination tasks of increasing complexity. These behavioral results confirm our model predictions, and provide the first experimental evidence for a proposed role of Heterosynaptic Plasticity in learning.
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Distinct Heterosynaptic Plasticity in Fast Spiking and Non-Fast-Spiking Inhibitory Neurons in Rat Visual Cortex.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2019Co-Authors: Marina Chistiakova, Nicholas M. Bannon, Vladimir Ilin, Matvey Roshchin, Alexey A. Malyshev, Zoltán F. Kisvárday, Maxim VolgushevAbstract:Inhibition in neuronal networks of the neocortex serves a multitude of functions, such as balancing excitation and structuring neuronal activity in space and time. Plasticity of inhibition is mediated by changes at both inhibitory synapses, as well as excitatory synapses on inhibitory neurons. Using slices from visual cortex of young male rats, we describe a novel form of Plasticity of excitatory synapses on inhibitory neurons, weight-dependent Heterosynaptic Plasticity. Recordings from connected pyramid-to-interneuron pairs confirm that postsynaptic activity alone can induce long-term changes at synapses that were not presynaptically active during the induction, i.e., Heterosynaptic Plasticity. Moreover, Heterosynaptic changes can accompany homosynaptic Plasticity induced in inhibitory neurons by conventional spike-timing-dependent Plasticity protocols. In both fast-spiking (FS) and non-FS neurons, Heterosynaptic changes were weight-dependent, because they correlated with initial paired-pulse ratio (PPR), indicative of initial strength of a synapse. Synapses with initially high PPR, indicative of low release probability (“weak” synapses), had the tendency to be potentiated, while synapses with low initial PPR (“strong” synapses) tended to depress or did not change. Interestingly, the net outcome of Heterosynaptic changes was different in FS and non-FS neurons. FS neurons expressed balanced changes, with gross average (n = 142) not different from control. Non-FS neurons (n = 66) exhibited net potentiation. This difference could be because of higher initial PPR in the non-FS neurons. We propose that weight-dependent Heterosynaptic Plasticity may counteract runaway dynamics of excitatory inputs imposed by Hebbian-type learning rules and contribute to fine-tuning of distinct aspects of inhibitory function mediated by FS and non-FS neurons in neocortical networks. SIGNIFICANCE STATEMENT Dynamic balance of excitation and inhibition is fundamental for operation of neuronal networks. Fine-tuning of such balance requires synaptic Plasticity. Knowledge about diverse forms of Plasticity operating in excitatory and inhibitory neurons is necessary for understanding normal function and causes of dysfunction of the nervous system. Here we show that excitatory inputs to major archetypal classes of neocortical inhibitory neurons, fast-spiking (FS) and non-fast-spiking (non-FS), express a novel type of Plasticity, weight-dependent Heterosynaptic Plasticity, which accompanies the induction of Hebbian-type changes. This novel form of Plasticity may counteract runaway dynamics at excitatory synapses to inhibitory neurons imposed by Hebbian-type learning rules and contribute to fine-tuning of diverse aspects of inhibitory function mediated by FS and non-FS neurons in neocortical networks.
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Adenosine Shifts Plasticity Regimes between Associative and Homeostatic by Modulating Heterosynaptic Changes.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016Co-Authors: Nicholas M. Bannon, Marina Chistiakova, Jen-yung Chen, Maxim Bazhenov, Maxim VolgushevAbstract:Endogenous extracellular adenosine level fluctuates in an activity-dependent manner and with sleep–wake cycle, modulating synaptic transmission and short-term Plasticity. Hebbian-type long-term Plasticity introduces intrinsic positive feedback on synaptic weight changes, making them prone to runaway dynamics. We previously demonstrated that co-occurring, weight-dependent Heterosynaptic Plasticity can robustly prevent runaway dynamics. Here we show that at neocortical synapses in slices from rat visual cortex, adenosine modulates the weight dependence of Heterosynaptic Plasticity: blockade of adenosine A1 receptors abolished weight dependence, while increased adenosine level strengthened it. Using model simulations, we found that the strength of weight dependence determines the ability of Heterosynaptic Plasticity to prevent runaway dynamics of synaptic weights imposed by Hebbian-type learning. Changing the weight dependence of Heterosynaptic Plasticity within an experimentally observed range gradually shifted the operating point of neurons between an unbalancing regime dominated by associative Plasticity and a homeostatic regime of tightly constrained synaptic changes. Because adenosine tone is a natural correlate of activity level (activity increases adenosine tone) and brain state (elevated adenosine tone increases sleep pressure), modulation of Heterosynaptic Plasticity by adenosine represents an endogenous mechanism that translates changes of the brain state into a shift of the regime of synaptic Plasticity and learning. We speculate that adenosine modulation may provide a mechanism for fine-tuning of Plasticity and learning according to brain state and activity. SIGNIFICANCE STATEMENT Associative learning depends on brain state and is impaired when the subject is sleepy or tired. However, the link between changes of brain state and modulation of synaptic Plasticity and learning remains elusive. Here we show that adenosine regulates weight dependence of Heterosynaptic Plasticity: adenosine strengthened weight dependence of Heterosynaptic Plasticity; blockade of adenosine A1 receptors abolished it. In model neurons, such changes of the weight dependence of Heterosynaptic Plasticity shifted their operating point between regimes dominated by associative Plasticity or by synaptic homeostasis. Because adenosine tone is a natural correlate of activity level and brain state, modulation of Plasticity by adenosine represents an endogenous mechanism for translation of brain state changes into a shift of the regime of synaptic Plasticity and learning.
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Partial Breakdown of Input Specificity of STDP at Individual Synapses Promotes New Learning.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2016Co-Authors: Maxim Volgushev, Marina Chistiakova, Jen-yung Chen, Vladimir Ilin, Roman Goz, Maxim BazhenovAbstract:Hebbian-type learning rules, which underlie learning and refinement of neuronal connectivity, postulate input specificity of synaptic changes. However, theoretical analyses have long appreciated that additional mechanisms, not restricted to activated synapses, are needed to counteract positive feedback imposed by Hebbian-type rules on synaptic weight changes and to achieve stable operation of learning systems. The biological basis of such mechanisms has remained elusive. Here we show that, in layer 2/3 pyramidal neurons from slices of visual cortex of rats, synaptic changes induced at individual synapses by spike timing-dependent Plasticity do not strictly follow the input specificity rule. Spike timing-dependent Plasticity is accompanied by changes in unpaired synapses: Heterosynaptic Plasticity. The direction of Heterosynaptic changes is weight-dependent, with balanced potentiation and depression, so that the total synaptic input to a cell remains preserved despite potentiation or depression of individual synapses. Importantly, this form of Heterosynaptic Plasticity is induced at unpaired synapses by the same pattern of postsynaptic activity that induces homosynaptic changes at paired synapses. In computer simulations, we show that experimentally observed Heterosynaptic Plasticity can indeed serve the theoretically predicted role of robustly preventing runaway dynamics of synaptic weights and activity. Moreover, it endows model neurons and networks with essential computational features: enhancement of synaptic competition, facilitation of the development of specific intrinsic connectivity, and the ability for relearning. We conclude that Heterosynaptic Plasticity is an inherent property of plastic synapses, crucial for normal operation of learning systems. SIGNIFICANCE STATEMENT We show that spike timing-dependent Plasticity in L2/L3 pyramids from rat visual cortex is accompanied by plastic changes in unpaired synapses. These Heterosynaptic changes are weight-dependent and balanced: individual synapses expressed significant LTP or LTD, but the average over all synapses did not change. Thus, the rule of input specificity breaks down at individual synapses but holds for responses averaged over many inputs. In model neurons and networks, this experimentally characterized form of Heterosynaptic Plasticity prevents runaway dynamics of synaptic weights and activity, enhances synaptic competition, facilitates development of specific intrinsic connectivity, and enables relearning. This new form of Heterosynaptic Plasticity represents the cellular basis of a theoretically postulated mechanism, which is additional to Hebbian-type rules, and is necessary for stable operation of learning systems.
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Homeostatic role of Heterosynaptic Plasticity: models and experiments.
Frontiers in computational neuroscience, 2015Co-Authors: Marina Chistiakova, Nicholas M. Bannon, Jen-yung Chen, Maxim Bazhenov, Maxim VolgushevAbstract:Homosynaptic Hebbian-type Plasticity provides a cellular mechanism of learning and refinement of connectivity during development in a variety of biological systems. In this review we argue that a complimentary form of Plasticity - Heterosynaptic Plasticity - represents a necessary cellular component for homeostatic regulation of synaptic weights and neuronal activity. The required properties of a homeostatic mechanism which acutely constrains the runaway dynamics imposed by Hebbian associative Plasticity have been well-articulated by theoretical and modeling studies. Such mechanism(s) should robustly support the stability of operation of neuronal networks and synaptic competition, include changes at non-active synapses, and operate on a similar time scale to Hebbian-type Plasticity. The experimentally observed properties of Heterosynaptic Plasticity have introduced it as a strong candidate to fulfill this homeostatic role. Subsequent modeling studies which incorporate Heterosynaptic Plasticity into model neurons with Hebbian synapses (utilizing an STDP learning rule) have confirmed its ability to robustly provide stability and competition. In contrast, properties of homeostatic synaptic scaling, which is triggered by extreme and long lasting (hours and days) changes of neuronal activity, do not fit two crucial requirements for a hypothetical homeostatic mechanism needed to provide stability of operation in the face of on-going synaptic changes driven by Hebbian-type learning rules. Both the trigger and the time scale of homeostatic synaptic scaling are fundamentally different from those of the Hebbian-type Plasticity. We conclude that Heterosynaptic Plasticity, which is triggered by the same episodes of strong postsynaptic activity and operates on the same time scale as Hebbian-type associative Plasticity, is ideally suited to serve homeostatic role during on-going synaptic Plasticity.
Nripan Mathews - One of the best experts on this subject based on the ideXlab platform.
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Ultralow Power Dual-Gated Subthreshold Oxide Neuristors: An Enabler for Higher Order Neuronal Temporal Correlations.
ACS nano, 2018Co-Authors: Rohit Abraham John, Nidhi Tiwari, Chen Yaoyi, Naveen Tiwari, Mohit Rameshchandra Kulkarni, Amoolya Nirmal, Anh Chien Nguyen, Arindam Basu, Ankit, Nripan MathewsAbstract:Inspired by neural computing, the pursuit of ultralow power neuromorphic architectures with highly distributed memory and parallel processing capability has recently gained more traction. However, emulation of biological signal processing via artificial neuromorphic architectures does not exploit the immense interplay between local activities and global neuromodulations observed in biological neural networks and hence are unable to mimic complex biologically plausible adaptive functions like Heterosynaptic Plasticity and homeostasis. Here, we demonstrate emulation of complex neuronal behaviors like Heterosynaptic Plasticity, homeostasis, association, correlation, and coincidence in a single neuristor via a dual-gated architecture. This multiple gating approach allows one gate to capture the effect of local activity correlations and the second gate to represent global neuromodulations, allowing additional modulations which augment their Plasticity, enabling higher order temporal correlations at a unitary level. Moreover, the dual-gate operation extends the available dynamic range of synaptic conductance while maintaining symmetry in the weight-update operation, expanding the number of accessible memory states. Finally, operating neuristors in the subthreshold regime enable synaptic weight changes with high gain while maintaining ultralow power consumption of the order of femto-Joules.
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ultralow power dual gated subthreshold oxide neuristors an enabler for higher order neuronal temporal correlations
ACS Nano, 2018Co-Authors: Rohit Abraham John, Nidhi Tiwari, Chen Yaoyi, Naveen Tiwari, Mohit Rameshchandra Kulkarni, Amoolya Nirmal, Anh Chien Nguyen, Arindam Basu, Nripan MathewsAbstract:Inspired by neural computing, the pursuit of ultralow power neuromorphic architectures with highly distributed memory and parallel processing capability has recently gained more traction. However, emulation of biological signal processing via artificial neuromorphic architectures does not exploit the immense interplay between local activities and global neuromodulations observed in biological neural networks and hence are unable to mimic complex biologically plausible adaptive functions like Heterosynaptic Plasticity and homeostasis. Here, we demonstrate emulation of complex neuronal behaviors like Heterosynaptic Plasticity, homeostasis, association, correlation, and coincidence in a single neuristor via a dual-gated architecture. This multiple gating approach allows one gate to capture the effect of local activity correlations and the second gate to represent global neuromodulations, allowing additional modulations which augment their Plasticity, enabling higher order temporal correlations at a unitary l...
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Ultralow Power Dual-Gated Subthreshold Oxide Neuristors: An Enabler for Higher Order Neuronal Temporal Correlations
2018Co-Authors: Rohit Abraham John, Nidhi Tiwari, Chen Yaoyi, Naveen Tiwari, Amoolya Nirmal, Anh Chien Nguyen, Arindam Basu, Mohit Kulkarni, Nripan MathewsAbstract:Inspired by neural computing, the pursuit of ultralow power neuromorphic architectures with highly distributed memory and parallel processing capability has recently gained more traction. However, emulation of biological signal processing via artificial neuromorphic architectures does not exploit the immense interplay between local activities and global neuromodulations observed in biological neural networks and hence are unable to mimic complex biologically plausible adaptive functions like Heterosynaptic Plasticity and homeostasis. Here, we demonstrate emulation of complex neuronal behaviors like Heterosynaptic Plasticity, homeostasis, association, correlation, and coincidence in a single neuristor via a dual-gated architecture. This multiple gating approach allows one gate to capture the effect of local activity correlations and the second gate to represent global neuromodulations, allowing additional modulations which augment their Plasticity, enabling higher order temporal correlations at a unitary level. Moreover, the dual-gate operation extends the available dynamic range of synaptic conductance while maintaining symmetry in the weight-update operation, expanding the number of accessible memory states. Finally, operating neuristors in the subthreshold regime enable synaptic weight changes with high gain while maintaining ultralow power consumption of the order of femto-Joules
Samuel Schacher - One of the best experts on this subject based on the ideXlab platform.
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Persistent Long-Term Facilitation at an Identified Synapse Becomes Labile with Activation of Short-Term Heterosynaptic Plasticity
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014Co-Authors: Samuel SchacherAbstract:Short-term and long-term synaptic Plasticity are cellular correlates of learning and memory of different durations. Little is known, however, how these two forms of Plasticity interact at the same synaptic connection. We examined the reciprocal impact of short-term Heterosynaptic or homosynaptic Plasticity at sensorimotor synapses of Aplysia in cell culture when expressing persistent long-term facilitation (P-LTF) evoked by serotonin [5-hydroxytryptamine (5-HT)]. Short-term Heterosynaptic Plasticity induced by 5-HT (facilitation) or the neuropeptide FMRFa (depression) and short-term homosynaptic Plasticity induced by tetanus [post-tetanic potentiation (PTP)] or low-frequency stimulation [homosynaptic depression (HSD)] of the sensory neuron were expressed in both control synapses and synapses expressing P-LTF in the absence or presence of protein synthesis inhibitors. All forms of short-term Plasticity failed to significantly affect ongoing P-LTF in the absence of protein synthesis inhibitors. However, P-LTF reversed to control levels when either 5-HT or FMRFa was applied in the presence of rapamycin. In contrast, P-LTF was unaffected when either PTP or HSD was evoked in the presence of either rapamycin or anisomycin. These results indicate that synapses expressing persistent Plasticity acquire a “new” baseline and functionally express short-term changes as naive synapses, but the new baseline becomes labile following selective activations—Heterosynaptic stimuli that evoke opposite forms of Plasticity—such that when presented in the presence of protein synthesis inhibitors produce a rapid reversal of the persistent Plasticity. Activity-selective induction of a labile state at synapses expressing persistent Plasticity may facilitate the development of therapies for reversing inappropriate memories.
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Differential distribution of functional receptors for neuromodulators evoking short-term Heterosynaptic Plasticity in Aplysia sensory neurons.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 1996Co-Authors: Zhong-yi Sun, Beth Kauderer, Samuel SchacherAbstract:Synaptic transmission and excitability in Aplysia sensory neurons (SNs) are bidirectionally modulated by 5-HT and FMRFamide. To explore the regional distribution of different functional receptors that modulate SN properties, we examined changes in synaptic efficacy and excitability with brief focal applications of the neuromodulators to different regions of SNs that have established connections with motor cell L7 in culture. Short-term changes in synaptic efficacy were evoked only when 5-HT or FMRFamide was applied to regions with SN varicosities along the surface of L7 axons. Applications to adjacent SN neurites with few varicosities in contact with L7 axons failed to evoke a significant change in synaptic efficacy. The distribution of functional receptors mediating changes in excitability differed for 5-HT and FMRFamide. Whereas excitability increases were evoked only when 5-HT was applied to SN cell bodies, excitability decreases in SNs were evoked only when FMRFamide was applied to regions along the L7 axon with SN varicosities. Without the target cell, cell bodies of SNs expressed both 5-HT and FMRFamide receptors that modulate excitability. These results indicate that functional G-protein-coupled receptors for two neuromodulators are distributed differentially along the surface of a presynaptic neuron that forms chemical connections in vitro . This differential distribution of receptors on the presynaptic neuron is regulated by a target and does not require the physical presence of neurons that release the neuromodulators.
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Inhibitors of protein and RNA synthesis block structural changes that accompany long-term Heterosynaptic Plasticity in Aplysia
Neuron, 1992Co-Authors: Craig H. Bailey, Eric R. Kandel, P.g. Montarolo, Mary Chen, Samuel SchacherAbstract:Synaptic connections between the sensory and motor neurons of Aplysia in culture undergo long-term facilitation in response to serotonin (5-HT) and long-term depression in response to FMRFamide. These long-term functional changes are dependent on the synthesis of macromolecules during the period in which the transmitter is applied and are accompanied by structural changes. There is an increase and a decrease, respectively, in the number of sensory neuron varicosities in response to 5-HT and FMRFamide. To determine whether macromolecular synthesis is also required for the structural changes, we examined in parallel the effects of inhibitors of protein (anisomycin) or RNA (actinomycin D) synthesis on the structural and functional changes. We have found that anisomycin and actinomycin D block both the enduring alterations in varicosity number and the long-lasting changes in synaptic potential. These results indicate that macromolecular synthesis is required for expression of the long-lasting structural changes in the sensory cells and that this synthesis is correlated with the long-term functional modulation of sensorimotor synapses.
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Target-dependent structural changes in sensory neurons of aplysia accompany long-term Heterosynaptic inhibition
Neuron, 1991Co-Authors: Samuel Schacher, P.g. MontaroloAbstract:FMRFamide evokes both short-term and long-term inhibition of synapses between mechanosensory and motor neurons in Aplysia. We report here, using dissociated cell culture and low-light epifluorescence video microscopy, that depression lasting 24 hr of sensorimotor synapses evoked by four brief applications of FMRFamide is accompanied by a significant loss of sensory cell varicosities and neurites. These structural changes in the sensory cells require the presence of the target motor cell L7. Because the loss of structures known to contain transmitter release sites correlates significantly with the changes in the amplitude of the excitatory postsynaptic potential in L7, our results suggest that the structural changes evoked by FMRFamide reflect a loss of synaptic contacts. Thus, long-term depression parallels long-term facilitation of the sensorimotor synapse produced by serotonin in that both forms of Heterosynaptic Plasticity involve target-dependent modulation of the number of presynaptic varicosities.
Rohit Abraham John - One of the best experts on this subject based on the ideXlab platform.
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Ultralow Power Dual-Gated Subthreshold Oxide Neuristors: An Enabler for Higher Order Neuronal Temporal Correlations.
ACS nano, 2018Co-Authors: Rohit Abraham John, Nidhi Tiwari, Chen Yaoyi, Naveen Tiwari, Mohit Rameshchandra Kulkarni, Amoolya Nirmal, Anh Chien Nguyen, Arindam Basu, Ankit, Nripan MathewsAbstract:Inspired by neural computing, the pursuit of ultralow power neuromorphic architectures with highly distributed memory and parallel processing capability has recently gained more traction. However, emulation of biological signal processing via artificial neuromorphic architectures does not exploit the immense interplay between local activities and global neuromodulations observed in biological neural networks and hence are unable to mimic complex biologically plausible adaptive functions like Heterosynaptic Plasticity and homeostasis. Here, we demonstrate emulation of complex neuronal behaviors like Heterosynaptic Plasticity, homeostasis, association, correlation, and coincidence in a single neuristor via a dual-gated architecture. This multiple gating approach allows one gate to capture the effect of local activity correlations and the second gate to represent global neuromodulations, allowing additional modulations which augment their Plasticity, enabling higher order temporal correlations at a unitary level. Moreover, the dual-gate operation extends the available dynamic range of synaptic conductance while maintaining symmetry in the weight-update operation, expanding the number of accessible memory states. Finally, operating neuristors in the subthreshold regime enable synaptic weight changes with high gain while maintaining ultralow power consumption of the order of femto-Joules.
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ultralow power dual gated subthreshold oxide neuristors an enabler for higher order neuronal temporal correlations
ACS Nano, 2018Co-Authors: Rohit Abraham John, Nidhi Tiwari, Chen Yaoyi, Naveen Tiwari, Mohit Rameshchandra Kulkarni, Amoolya Nirmal, Anh Chien Nguyen, Arindam Basu, Nripan MathewsAbstract:Inspired by neural computing, the pursuit of ultralow power neuromorphic architectures with highly distributed memory and parallel processing capability has recently gained more traction. However, emulation of biological signal processing via artificial neuromorphic architectures does not exploit the immense interplay between local activities and global neuromodulations observed in biological neural networks and hence are unable to mimic complex biologically plausible adaptive functions like Heterosynaptic Plasticity and homeostasis. Here, we demonstrate emulation of complex neuronal behaviors like Heterosynaptic Plasticity, homeostasis, association, correlation, and coincidence in a single neuristor via a dual-gated architecture. This multiple gating approach allows one gate to capture the effect of local activity correlations and the second gate to represent global neuromodulations, allowing additional modulations which augment their Plasticity, enabling higher order temporal correlations at a unitary l...