Search results for 'LTP' (try it on Scholar)

48 found
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  1.  3
    Sverker Sikström (2006). The Isolation, Primacy, and Recency Effects Predicted by an Adaptive LTD/LTP Threshold in Postsynaptic Cells. Cognitive Science 30 (2):243-275.
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  2.  32
    John Bickle (2002). Concepts Structured Through Reduction: A Structuralist Resource Illuminates the ConsolidationLong-Term Potentiation (Ltp) Link. Synthese 130 (1):123 - 133.
    The structuralist program has developed a useful metascientific resource: ontological reductive links (ORLs) between the constituents of the potential models of reduced and reducing theories. This resource (...)
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  3.  7
    Jerry W. Rudy & Julian R. Keith (1997). LTP and Memory: Déjà Vu. Behavioral and Brain Sciences 20 (4):629-629.
    Shors & Matzel's conclusion that LTP is not related to learning is similar to one we reached several years ago. We discuss some methodological advances that have (...)
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  4.  6
    Klaus G. Reymann (1997). As in Long-Term Memory, LTP is Consolidated by Reinforcers. Behavioral and Brain Sciences 20 (4):627-628.
    Recent evidence from our lab indicates that LTP shares an important property with memory consolidation: it is consolidated by natural reinforcement. Nevertheless, the hypothesis, that LTP-like (...)mechanisms or other forms of enhanced synaptic efficacy are basic elements in learning is not unequivocally supported. Skepticism aside, LTP is an accessible experimental model that is optimally equipped for the investigation of the cellular and molecular machinery involved in synaptic weight changes. (shrink)
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  5.  16
    Lev P. Latash (1997). LTP is Neither a Memory Trace nor an Ultimate Mechanism for its Formation: The Beginning of the End of the Synaptic Theory of Neural Memory. Behavioral and Brain Sciences 20 (4):621-622.
    The problem of neural memory storage is discussed, based on the results of studies of memory impairment after hippocampal lesions, motor learning, and electrophysiological research onspinal (...)
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  6.  12
    Tracey J. Shors & Louis D. Matzel (1997). LTP: Memory, Arousal, Neither, Both. Behavioral and Brain Sciences 20 (4):634-645.
    The neurophysiological phenomenon of LTP (long term potentiation) is considered by many to represent an adequate mechanism for acquiring or storing memories in the mammalian brain. In (...)
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  7.  10
    Stephen Maren (1997). Arousing the LTP and Learning Debate. Behavioral and Brain Sciences 20 (4):622-623.
    Shors & Matzel provide compelling arguments against a role for hippocampal long-term potentiation (LTP) in mammalian learning and memory. As an alternative, they suggest that LTP is (...)
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  8.  11
    Tracey J. Shors & Louis D. Matzel (2000). The Status of LTP as a Mechanism of Memory Formation in the Mammalian Brain. Behavioral and Brain Sciences 23 (2):288-290.
    Long-term potentiation (LTP) is a long-lasting increase in synaptic efficacy that many consider the best candidate currently available for a neural mechanism of memory formation and (...)/or storage in the mammalian brain. In our target article, LTP: What's learning got to do with it?, we concluded that there was insufficient data to warrant such a conclusion. In their commentaries, Jeffery and Zhadin raise a number of important issues that we did not raise, both for and against the hypothesis. Although we agree with a number of these issues, we maintain that there remains insufficient evidence that LTP is a memory mechanism. (shrink)
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  9.  6
    Robert D. Hawkins (1997). LTP and Learning: Let's Stay Together. Behavioral and Brain Sciences 20 (4):620-621.
    The hypothesis that there is a 1:1 correspondence between LTP and learning is simplistic, and the correlation approach to testing it is therefore too limited. The (...)alternative hypothesis that LTP plays a role in arousal is consistent with activity-dependent neuromodulation, but ignores the Hebbian properties of LTP. LTP may involve both types of mechanisms, suggesting a possible synthesis of the two hypotheses. (shrink)
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  10.  9
    Ken-ichi Hara & Tatsuo Kitajima (1997). LTP Plays a Distinct Role in Various Brain Structures. Behavioral and Brain Sciences 20 (4):620-620.
    LTP is thought to be an experimental model for studying the cellular mechanism of learning and memory. Shors & Matzel review some contradictory data concerning the linkage between (...) LTP and memory and suggest that LTP does not underlie learning and memory. LTP is a cellular and synaptic process and cannot be a memory mechanism. In fact, it is a cellular information storage mechanism. (shrink)
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  11.  5
    Christopher I. Moore & Mriganka Sur (1997). Cortical Plasticity and LTP. Behavioral and Brain Sciences 20 (4):623-624.
    In the developing and adult cortex, just as in the adult hippocampus, LTP is unable to account for a variety of types of functional plasticity.
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  12.  6
    Michael S. Fanselow (1997). Without LTP the Learning Circuit is Broken. Behavioral and Brain Sciences 20 (4):616-616.
    Since learning emerges from a circuit mediating behavior it is unrealistic to require LTP to be a sufficient explanation of it; however, LTP is a necessary component (...)
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  13.  5
    Robert Gerlai (1997). A Causal Relationship Between LTP and Learning? Has the Question Been Answered by Genetic Approaches? Behavioral and Brain Sciences 20 (4):617-618.
    Gene targeting has generated a great deal of data on the molecular mechanisms of long-term potentiation and its potential role in learning and memory. However, the (...)interpretation of some results has been questioned. Compensatory mechanisms and the contribution of genetic background may make it difficult to unequivocally prove the existence of a causal (genetic) link between LTP and learning. (shrink)
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  14.  2
    Richard F. Thompson (1997). Classical Conditioning has Much to Do with LTP. Behavioral and Brain Sciences 20 (4):632-633.
    Shors & Matzel somewhat lightly dismiss the evidence that a process like LTP may underlie the learning-induced increase in neuronal activity in the hippocampus in eyeblink conditioning. (...)
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  15.  2
    Clive R. Bramham (1997). State-Dependent Suppression of LTP Induction After Learning: Relation to Phasic Hippocampal Network Events. Behavioral and Brain Sciences 20 (4):614-615.
    This commentary argues that (1) arousal is not sufficient to induce LTP in the hippocampus, (2) learning can profoundly modulate synaptic plasticity in a state-dependent manner (...)without affecting baseline synaptic efficacy, and (3) unilateral, synapse-specific LTP induction triggers an interhippocampal communication manifested as bilateral increases in gene expression at multiple sites in the hippocampal network. (shrink)
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  16.  6
    I. C. Reid & C. A. Stewart (1997). Stress, LTP, and Depressive Disorder. Behavioral and Brain Sciences 20 (4):626-627.
    Preoccupation with LTP as a putative memory mechanism may have retarded the consideration of pathological modulation of synaptic plasticity in clinical disorders where memory dysfunction is not (...)
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  17.  4
    Kathryn J. Jeffery (2000). LTPa Mechanism in Search of a Function. Behavioral and Brain Sciences 23 (2):286-287.
    Shors & Matzel (1997) suggest replacing the questionIs LTP a mechanism of learning?” withIs LTP a mechanism of arousal and attention?” However, the failure of experiments (...) to verify the LTP-learning hypothesis may arise not because it is untrue, but because in its current guise, it is not properly testable. If so, then the LTP-attention hypothesis is untestable, as well. (shrink)
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  18.  3
    Donald Peter Cain (1997). Importance of Behaviour in LTP Research. Behavioral and Brain Sciences 20 (4):615-616.
    Shors and Matzel's evaluation of approaches to the behavioural function of LTP is welcome, and should encourage a widening of conceptual approaches to this problem. In (...)addition to their call for increased sophistication in thinking about LTP, there needs to be a parallel increase in sophistication in the study of behaviour. Changes in emotional state or tone may be a better function for LTP than attention mechanisms. (shrink)
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  19.  3
    Mikhail N. Zhadin (2000). LTP and Reinforcement: Possible Role of the Monoaminergic Systems. Behavioral and Brain Sciences 23 (2):287-288.
    The absence of a clear influence of the responses modified by new connections created by LTP on the development of these connections casts doubt on an essential (...)
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  20.  1
    Wickliffe C. Abraham (1997). Keeping Faith with the Properties of LTP. Behavioral and Brain Sciences 20 (4):614-614.
    Despite close scrutiny in recent years, the traditional properties of LTP are holding up remarkably well, and they remain a credible influence on the belief that LTP (...)
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  21.  12
    Maurice K. D. Schouten & Huib Looren De Jong (1999). Reduction, Elimination, and Levels: The Case of the LTP-Learning Link. Philosophical Psychology 12 (3):237 – 262.
    We argue in this paper that so-called new wave reductionism fails to capture the nature of the interlevel relations between psychology and neuroscience. Bickle (1995, Psychoneural (...)reduction of the genuinely cognitive: some accomplished facts, Philosophical Psychology, 8, 265-285; 1998, Psychoneural reduction: the new wave, Cambridge, MA: MIT Press) has claimed that a (bottom-up) reduction of the psychological concepts of learning and memory to the concepts of neuroscience has in fact already been accomplished. An investigation of current research on the phenomenon of long-term potentiation reveals that this claim overstates the facts. Both the psychological and the neural concepts involved have not yet stabilized and face further correction under the influence of both bottom-up and top-down selection pressures. In addition, psychological concepts often refer to functions, and functions are indispensable and irreducible. Function ascriptions pick out objective patterns involving historical factors and distal goals. This view of functions implies that psychological facts cannot be simply read off from the neurophysiological facts. Although psychological theorizing is constrained by neurophysiology (and vice versa), psychology remains distinct at least to some degree. (shrink)
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  22.  4
    Peter V. Nguyen (2002). All Spaced Out Over Memory and LTP. Trends in Cognitive Sciences 6 (8):330.
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  23.  5
    C. H. Vanderwolf (1997). Hippocampus and LTP: Here We Go Around Again. Behavioral and Brain Sciences 20 (4):633-634.
    A fundamental assumption in Shors & Matzel's target article is that brain activity can be related to the traditional categories of mentalistic psychology. This has led them (...)
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  24.  5
    Erik D. Roberson & J. David Sweatt (1995). Regulation of Adenylyl Cyclase in LTP. Behavioral and Brain Sciences 18 (3):485-486.
    Our results on hippocampal long-term potentiation are considered in the context of Xia et al.'s hypothesis. Whereas the target article proposes presynaptic PKC involvement in adenylyl (...) cyclase activation by phosphorylation of nenromodulin, we suggest an additional postsynaptic role involving RC3/nenrogranin. Finally, we examine the possibility that the adenylyl cyclase mutant mouse may display normal learning with a selective impairment of memory. (shrink)
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  25.  6
    Zhengui Xia & Daniel R. Storm (1995). Evidence That the Type I Adenylyl Cyclase May Be Important for Neuroplasticity: Mutant Mice Deficient in the Gene for Type I Adenylyl Cyclase Show Altered Behavior and LTP. Behavioral and Brain Sciences 18 (3):498-500.
    The regulatory properties of the neurospecific, type I adenylyl cyclase and its distribution within brain have suggested that this enzyme may be important for neuroplasticity. To address (...)
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  26.  1
    Michel Baudry (1996). Similarities and Contrasts Between Cerebellar LTD and Hippocampal LTP. Behavioral and Brain Sciences 19 (3):435-436.
    In this commentary, I review the articles by CrPEL et al.; LINDEN; Vincent].
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  27. Pegado Felipe, Boets Bart & Op De Beeck Hans (2014). Implicit Manipulation of Face Processing Performance with LTP/LTD-Like Visual Stimulation. Frontiers in Human Neuroscience 8.
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  28. Pegado Felipe, Boets Bart & OpDeBeeck Hans (2015). Passively Improving Face Processing with LTP-Like Visual Stimulation. Frontiers in Human Neuroscience 9.
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  29. Stefan Klöppel, Eliza Lauer, Jessica Peter, Lora Minkova, Christoph Nissen, Claus Normann, Janine Reis, Florian Mainberger, Michael Bach & Jacob Lahr (2015). LTP-Like Plasticity in the Visual System and in the Motor System Appear Related in Young and Healthy Subjects. Frontiers in Human Neuroscience 9.
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  30. John Bickle (2006). Reducing Mind to Molecular Pathways: Explicating the Reductionism Implicit in Current Cellular and Molecular Neuroscience. [REVIEW] Synthese 151 (3):411-434.
    As opposed to the dismissive attitude toward reductionism that is popular in current philosophy of mind, aruthless reductionismis alive and thriving inmolecular and cellular (...)
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  31.  64
    Carl F. Craver (2003). The Making of a Memory Mechanism. Journal of the History of Biology 36 (1):153-95.
    Long-Term Potentiation (LTP) is a kind of synaptic plasticity that many contemporary neuroscientists believe is a component in mechanisms of memory. This essay describes the discovery (...)of LTP and the development of the LTP research program. The story begins in the 1950's with the discovery of synaptic plasticity in the hippocampus (a medial temporal lobe structure now associated with memory), and it ends in 1973 with the publication of three papers sketching the future course of the LTP research program. The making of LTP was a protracted affair. Hippocampal synaptic plasticity was initially encountered as an experimental tool, then reported as a curiosity, and finally included in the ontic store of the neurosciences. Early researchers were not investigating the hippocampus in search of a memory mechanism; rather, they saw the hippocampus as a useful experimental model or as a structure implicated in the etiology of epilepsy. The link between hippocampal synaptic plasticity and learning or memory was a separate conceptual achievement. That link was formulated in at least three different ways at different times: reductively (claiming that plasticity is identical to learning), analogically (claiming that plasticity is an example or model of learning), and mechanistically (claiming that plasticity is a component in learning or memory mechanisms). The hypothesized link with learning or memory, coupled with developments in experimental techniques and preparations, shaped how researchers understood LTP itself. By 1973, the mechanistic formulation of the link between LTP and memory provided an abstract framework around which findings from multiple perspectives could be integrated into a multifield research program. (shrink)
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  32.  23
    Tracey J. Shors & Louis D. Matzel (1997). Long-Term Potentiation: What's Learning Got to Do with It? Behavioral and Brain Sciences 20 (4):597-614.
    Long-term potentiation (LTP) is operationally defined as a long-lasting increase in synaptic efficacy following high-frequency stimulation of afferent fibers. Since the first full description of (...)
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  33.  21
    Kenneth Sufka (2000). Chronic Pain Explained. Brain and Mind 1 (2):155-179.
    Pains that persist long after damaged tissue hasrecovered remain a perplexing phenomenon. Theseso-called chronic pains serve no useful function foran organism and, given its disabling effects, (...)mighteven be considered maladaptive. However, a remarkablesimilarity exists between the neural bases thatunderlie the hallmark symptoms of chronic pain andthose that subserve learning and memory. Bothphenomena, wind-up in the pain literature andlong-term potentiation (LTP) in the learning andmemory literature, are forms of neuroplasticity inwhich increased neural activity leads to a longlasting increase in the excitability of neuronsthrough structural modifications at pre- andpost-synaptic sites. Moreover, the synapticmodifications of wind-up and LTP share a commonmechanism: a glutamate N -methyl-D-aspartate(NMDA) receptor interaction that initiates a calciummediated biochemical cascade that ultimately enhancessignal processing at the -amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptor. This paper arguesthat chronic pain, which has no adaptive value, canbe accounted for in terms of the highly adaptivephenomenon of activity-dependent neural plasticity;hence, some cases of chronic pain can beconceptualized as a memory trace in spinal neurons. (shrink)
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  34.  27
    Clive R. Bramham (2005). Molecular Mechanisms of Synaptic Consolidation During Sleep: BDNF Function and Dendritic Protein Synthesis. Behavioral and Brain Sciences 28 (1):65-66.
    Insights into the role of sleep in the molecular mechanisms of memory consolidation may come from studies of activity-dependent synaptic plasticity, such as long-term potentiation (LTP (...)). This commentary posits a specific contribution of sleep to LTP stabilization, in which mRNA transported to dendrites during wakefulness is translated during sleep. Brain-derived neurotrophic factor may drive the translation of newly transported and resident mRNA. (shrink)
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  35.  4
    Warren Heideman (1995). Long Term Potentiation and CaM-Sensitive Adenylyl Cyclase: Long-Term Prospects. Behavioral and Brain Sciences 18 (3):477-478.
    The type I CaM-sensitive adenylyl cyclase is in a position to integrate signals from multiple inputs, consistent with the requirements for mediating long term potentiation (LTP). (...)Biochemical and genetic evidence supports the idea that this enzyme plays an important role inc LTP. However, more work is needed before we will be certain of the role that CaM-sensitive adenylyl cyclases play in LTP. (shrink)
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  36.  5
    David L. Walker & Paul E. Gold (1997). NMDA Receptors: Substrates or Modulators of Memory Formation. Behavioral and Brain Sciences 20 (4):634-634.
    We agree with Shors & Matzel's general hypothesis that the proposed link between NMDA-dependent LTP and memory is weak. They suggest that NMDA-dependent LTP is important (...) to arousal or attentional processes which influence learning in an anterograde manner. However, current evidence is also consistent with the view that NMDA receptors modulate memory consolidation retroactively, as occurs in several other receptor classes. (shrink)
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  37.  4
    Jonathan C. Gewirtz & Michael Davis (1997). Beyond Attention: The Role of Amygdala NMDA Receptors in Fear Conditioning. Behavioral and Brain Sciences 20 (4):618-619.
    Several types of amygdala-dependent learning can be blocked by local infusion of NMDA antagonists into the amygdala. This blockade shows anatomical, pharmacological, temporal, and behavioral specificity, (...)providing a pattern of data more consistent with a role for NMDA receptors in learning than in arousal or attention, and supporting the contention that anLTP-likeprocess is a neural substrate for memory formation. (shrink)
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  38.  6
    Zhengui Xia, Eui-Ju Choi, Daniel R. Storm & Christine Blazynski (1995). Do the Calmodulin-Stimulated Adenylyl Cyclases Play a Role in Neuroplasticity? Behavioral and Brain Sciences 18 (3):429-440.
    Evidence from invertebrate systems including Aplysia and Drosophila, as well as studies carried out with mammalian brain, suggests that Ca2+-sensitive adenylyl cyclases may be important for (...)long-term synaptic changes and learning and memory. Furthermore, some forms of long-term potentiation (LTP) in the hippocampus elevate cyclic AMP (cAMP) signals, and activation of adenylyl cyclases and cAMP-dependent protein kinase may be required for late stages of LTP. We propose that long-term changes in neurons and at synapses may require synergism between the cAMP and Ca2+ signal transduction systems which regulates transcription and synthesis of specific proteins required for long-term synaptic changes. During LTP, protein kinase C is activated and intraccllular Ca2+ increases. We hypothesize that the calmodulin (CaM)-regulated adenylyl cyclases may be activated during LTP because of increases in intracellular Ca2+, release of free CaM from neuromodulin, activation by protein kinase C, release of neurotransmitters, or a combination of these events. Synergistic activation of CaM-sensitive adenylyl cyclases may produce a robust or prolonged cAMP signal required for transcriptional control. Furthermore, the coupling of the Ca2+ and cAMP systems may provide positive feedback regulation of Ca2+ channels by cAMP-dependent protein kinase. (shrink)
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  39.  12
    Stephen Grossberg (1997). Adaptive Timing, Attention, and Movement Control. Behavioral and Brain Sciences 20 (4):619-619.
    Examples of how LTP and LTD can control adaptively-timed learning that modulates attention and motor control are given. It is also suggested that LTP/LTD can play (...) a role in storing memories. The distinction between match-based and mismatch-based learning may help to clarify the difference. (shrink)
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  40.  8
    Matthew Shapiro & Eric Hargreaves (1997). Long Term Potentiation: Attending to Levels of Organization of Learning and Memory Mechanisms. Behavioral and Brain Sciences 20 (4):631-632.
    Shors & Matzel set up a straw man, that LTP is a memory storage mechanism, and knock him down without due consideration of the important relations among different (...) levels of organization and analysis regarding LTP, learning, and memory. Assessing these relationships requires analysis and hypotheses linking specific brain regions, neural circuits, plasticity mechanisms, and task demands. The issue addressed by the authors is important, but their analysis is off target. (shrink)
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  41.  9
    Peter M. Milner (1997). Repetition Priming: Memory or Attention? Behavioral and Brain Sciences 20 (4):623-623.
    There is no general agreement as to the meaning of long-term potentiation, but this cannot be resolved by using it to explain additional phenomena. Increased attention (...)to recently experienced stimuli is a form of learning known to neuropsychologists as repetition priming. As more is learned about the neurochemistry of synaptic change, the term LTP will wither. (shrink)
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  42.  5
    Michel Dufossé, Arthur Kaladjian & Philippe Grandguillaume (1997). Origin of Error Signals During Cerebellar Learning of Motor Sequences. Behavioral and Brain Sciences 20 (2):249-250.
    Prefrontal cerebral areas project to Purkinje cells, located in the most lateral part of the cerebellum, via mossy and climbing fibers. The latter olivary error signals reflect (...)
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  43.  4
    Nestor A. Schmajuk (1997). Stimulus Configuration, Long-Term Potentiation, and the Hippocampus. Behavioral and Brain Sciences 20 (4):629-631.
    Shors & Matzel propose that hippocampal LTP increases the effective salience of discrete external stimuli and thereby facilitates the induction of memories at distant places. In line with (...) this suggestion, a neural network model of associative learning and hippocampal function assumes that LTP increases hippocampal error signals to the cortex, thereby facilitating stimulus configuration in association cortex. Computer simulations show that under these assumptions the model correctly describes the effect of LTP induction and blockade in classical discriminations and place learning. (shrink)
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  44.  2
    G. B. Robinson (1997). Learning and Synaptic Plasticity. Behavioral and Brain Sciences 20 (4):628-628.
    Controversy surrounds several experiments that have addressed whether selective synaptic strengthening occurs during learning. To date, the evidence suggests that widespread alterations in synaptic strength, through either (...)
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  45.  2
    Kjell Hole, Frode Svendsen & Arne Tjølsen (1997). Is Learning Involved in Plasticity in Nociceptive Regulation? Behavioral and Brain Sciences 20 (3):452-453.
    Plastic changes in spinal cord function like neuronal wind-up and increased receptive field are too short-lived to explain chronic pain without structural changes. It is possible (...) that learning could be a mechanism for longlasting changes in nociceptive regulation. A learning process localized to the spinal cord has been shown to be important for the development of tolerance to the analgetic effect of ethanol, suggesting that nociceptive control systems may be changed by learning. Long term potentiation (LTP) is regarded as a useful model of learning and memory. LTP-like changes have been observed in invitro preparations from the spinal cord and in spinal cord field potentials. Recently a long term increase in spinal A-[beta] and C-fibre evoked responses after painful stimulation has been observed. [coderre & katz, dickenson, wiesenfeld-hallin et al.]. (shrink)
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  46.  1
    Richard G. M. Morris (1997). Preconceptions and Prerequisites: Understanding the Function of Synaptic Plasticity Will Also Depend on a Better Systems-Level Understanding of the Multiple Types of Memory. Behavioral and Brain Sciences 20 (4):624-625.
    Although it is not their fault, Shors & Matzel's attempt to review the LTP and learning hypothesis suffers from there being no clear published statement of the (...)
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  47. Timothy Bliss, Graham Collingridge & Richard Morris (eds.) (2004). Long-Term Potentiation: Enhancing Neuroscience for 30 Years. Oxford University Press Uk.
    In the thirty years since its discovery by Terje Lomo and Tim Bliss, Long Term Potentiation has become one of the most extensively studied topics in contemporary (...)
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  48. Byunghan Kim (2013). The Lascar Group and the Strong Types of Hyperimaginaries. Notre Dame Journal of Formal Logic 54 (3-4):497-507.
    This is an expository note on the Lascar group. We also study the Lascar group over hyperimaginaries and make some new observations on the strong types over (...)
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