Long-term potentiation: Does it deserve attention?

1997 ◽  
Vol 20 (4) ◽  
pp. 625-626
Author(s):  
Shane M. O'Mara ◽  
Sean Commins ◽  
Colin Gemmell ◽  
John Gigg
Keyword(s):  
Hippocampal Neurons ◽  
Long Term Potentiation ◽  
Memory Storage ◽  
Storage Mechanism ◽  
Term Potentiation ◽  
Target Article ◽  
Arousal Mechanism

Shors & Matzel's target article is a thought-provoking attempt to reconceptualise long-term potentiation as an attentional or arousal mechanism rather than a memory storage mechanism. This is incompatible with the facts of the neurobiology of attention and of the behavioural neurophysiological properties of hippocampal neurons.

LTP: Memory, arousal, neither, both

1997 ◽  
Vol 20 (4) ◽  
pp. 634-645 ◽  
Author(s):  
Tracey J. Shors ◽  
Louis D. Matzel
Keyword(s):  
Long Term Potentiation ◽  
Memory Systems ◽  
Alternative Interpretation ◽  
Memory Storage ◽  
Mammalian Brain ◽  
Storage Device ◽  
Term Potentiation ◽  
Target Article ◽  
Mechanisms Of Memory

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 our target article, we reviewed the various arguments put forth in support of the LTP/memory hypothesis. We concluded that these arguments were inconsistent with the purported data base and proposed an alternative interpretation that we suggested was at least as compatible with the available data as the more widely held view. In doing so, we attempted to illustrate that the inadequacy of present experimental designs did not permit us to distinguish between equally viable hypotheses. In the four years since we wrote the first draft of our target article, hundreds of additional studies on LTP have been published and their results have been incorporated into current theories about memory. A diverse group of commentators responded to our target article with their own theories of how memories might be stored in the brain, some of which rely on LTP. Some commentators doubted whether memories can be stored through modifications of synaptic strength. Some assert that it will never be possible to understand the neural mechanisms of memory; still others remain hopeful that we will accomplish some semblance of a resolution, provided we appreciate LTP's role in a subset of seemingly amorphous memory systems. In summary, although it is commonly written that “LTP is a memory storage device,” the divergence of views among the commentators suggests, at least as strongly as our target article, that such conviction is unwarranted and fails to acknowledge both the lack of consensus regarding the role of LTP in memory and the complexity of the phenomenon of memory itself.

Long-term potentiation: What's learning got to do with it?

1997 ◽  
Vol 20 (4) ◽  
pp. 597-614 ◽  
Author(s):  
Tracey J. Shors ◽  
Louis D. Matzel
Keyword(s):  
Empirical Evidence ◽  
Long Term Potentiation ◽  
Memory Formation ◽  
Memory Storage ◽  
Storage Device ◽  
Full Description ◽  
High Frequency Stimulation ◽  
Term Potentiation ◽  
Target Article

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 the phenomenon in 1973, exploration of the mechanisms underlying LTP induction has been one of the most active areas of research in neuroscience. Of principal interest to those who study LTP, particularly in the mammalian hippocampus, is its presumed role in the establishment of stable memories, a role consistent with “Hebbian” descriptions of memory formation. Other characteristics of LTP, including its rapid induction, persistence, and correlation with natural brain rhythms, provide circumstantial support for this connection to memory storage. Nonetheless, there is little empirical evidence that directly links LTP to the storage of memories. In this target article we review a range of cellular and behavioral characteristics of LTP and evaluate whether they are consistent with the purported role of hippocampal LTP in memory formation. We suggest that much of the present focus on LTP reflects a preconception that LTP is a learning mechanism, although the empirical evidence often suggests that LTP is unsuitable for such a role. As an alternative to serving as a memory storage device, we propose that LTP may serve as a neural equivalent to an arousal or attention device in the brain. Accordingly, LTP may increase in a nonspecific way the effective salience of discrete external stimuli and may thereby facilitate the induction of memories at distant synapses. Other hypotheses regarding the functional utility of this intensely studied mechanism are conceivable; the intent of this target article is not to promote a single hypothesis but rather to stimulate discussion about the neural mechanisms underlying memory storage and to appraise whether LTP can be considered a viable candidate for such a mechanism.

Variations in Synaptic Plasticity and Types of Memory in Corticohippocampal Networks

1992 ◽  
Vol 4 (3) ◽  
pp. 189-199 ◽  
Author(s):  
Gary Lynch ◽  
Richard Granger
Keyword(s):  
Synaptic Plasticity ◽  
Assembly Line ◽  
Long Term Potentiation ◽  
Memory Storage ◽  
Storage Mechanism ◽  
Behavioral Studies ◽  
Term Potentiation ◽  
Unique Aspect

If Synaptic long-term potentiation (LTP) represents a memory storage mechanism, its induction and expression characteristics may constitute rules governing encoding and read-out of memory in cortical circuitry, The presence of variants of the LTP effect in different anatomical networks provides grounds for predictions about the types of memory operations to which potentiation contributes. Computer modeling studies incorporating the complex rules for LTP induction and the characteristics of expressed potentiation can be used to make such predictions specific. We review ttie types of synaptic plasticity found in the successive stages of the corticohippocampal pathway, and present results indicating that LTP does participate in definably different forms of memory, suggesting a classification of memory types differing somewhat from categories deduced from behavioral studies. Specifically, the results suggest that subtypes of memory operate serially, in an “assembly line” of specialized functions, each of which adds a unique aspect to the processing of memories. The effects of lesions on the encoding versus expression of memory can be interpreted from the perspective of this hypothesis.

Long term potentiation: Attending to levels of organization of learning and memory mechanisms

1997 ◽  
Vol 20 (4) ◽  
pp. 631-632
Author(s):  
Matthew Shapiro ◽  
Eric Hargreaves
Keyword(s):  
Learning And Memory ◽  
Long Term Potentiation ◽  
Brain Regions ◽  
Task Demands ◽  
Memory Storage ◽  
Storage Mechanism ◽  
Levels Of Organization ◽  
Term Potentiation ◽  
Set Up

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.

Arousing the LTP and learning debate

1997 ◽  
Vol 20 (4) ◽  
pp. 622-623 ◽  
Author(s):  
Stephen Maren
Keyword(s):  
Learning And Memory ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Arousal Mechanism

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 an arousal mechanism. I will argue that this view is not a satisfactory alternative to current conceptions of LTP function.

scholarly journals Selective increase of functional network connectivity in Arc-positive neuronal engrams after long-term potentiation

2020 ◽  
Author(s):  
Yuheng Jiang ◽  
Antonius M.J. VanDongen
Keyword(s):  
Functional Connectivity ◽  
Hippocampal Neurons ◽  
Network Effects ◽  
Network Connectivity ◽  
Long Term Potentiation ◽  
Early Gene ◽  
Memory Traces ◽  
Term Potentiation ◽  
Memory Engram

ABSTRACTNew tools in optogenetics and molecular biology have culminated in recent studies which mark immediate-early gene (IEG)-expressing neurons as memory traces or engrams. Although the activity-dependent expression of IEGs has been successfully utilised to label memory traces, their roles in engram specification is incompletely understood. Outstanding questions remain as to whether expression of IEGs can interplay with network properties such as functional connectivity and also if neurons expressing different IEGs are functionally distinct. We investigated the expression of Arc and c-Fos, two commonly utilised IEGs in memory engram specification, in cultured hippocampal neurons. After pharmacological induction of long-term potentiation (LTP) in the network, we noted an emergent network property of refinement in functional connectivity between neurons, characterized by a global down-regulation of network connectivity, together with strengthening of specific connections. Subsequently, we show that Arc expression correlates with the effects of network refinement, with Arc-positive neurons being selectively strengthened. Arc positive neurons were also found to be located in closer physical proximity to each other in the network. While the expression pattern of IEGs c-Fos and Arc strongly overlaps, Arc was more selectively expressed than c-Fos. These IEGs also act together in coding information about connection strength pruning. These results demonstrate important links between IEG expression and network connectivity, which serve to bridge the gap between cellular correlates and network effects in learning and memory.

scholarly journals Microtubule‐associated protein 2 mediates induction of long‐term potentiation in hippocampal neurons

2020 ◽  
Vol 34 (5) ◽  
pp. 6965-6983 ◽  
Author(s):  
Yoonju Kim ◽  
You‐Na Jang ◽  
Ji‐Young Kim ◽  
Nari Kim ◽  
Seulgi Noh ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Long Term Potentiation ◽  
Term Potentiation

scholarly journals Chemical LTD, but not LTP, induces transient accumulation of gelsolin in dendritic spines

2019 ◽  
Vol 400 (9) ◽  
pp. 1129-1139 ◽  
Author(s):  
Iryna Hlushchenko ◽  
Pirta Hotulainen
Keyword(s):  
Synaptic Plasticity ◽  
Dendritic Spines ◽  
Hippocampal Neurons ◽  
Long Term Potentiation ◽  
Excitatory Synapses ◽  
Signal Molecule ◽  
Brain Functions ◽  
Dendritic Shaft ◽  
Term Potentiation

Abstract Synaptic plasticity underlies central brain functions, such as learning. Ca2+ signaling is involved in both strengthening and weakening of synapses, but it is still unclear how one signal molecule can induce two opposite outcomes. By identifying molecules, which can distinguish between signaling leading to weakening or strengthening, we can improve our understanding of how synaptic plasticity is regulated. Here, we tested gelsolin’s response to the induction of chemical long-term potentiation (cLTP) or long-term depression (cLTD) in cultured rat hippocampal neurons. We show that gelsolin relocates from the dendritic shaft to dendritic spines upon cLTD induction while it did not show any relocalization upon cLTP induction. Dendritic spines are small actin-rich protrusions on dendrites, where LTD/LTP-responsive excitatory synapses are located. We propose that the LTD-induced modest – but relatively long-lasting – elevation of Ca2+ concentration increases the affinity of gelsolin to F-actin. As F-actin is enriched in dendritic spines, it is probable that increased affinity to F-actin induces the relocalization of gelsolin.

Reexamination of the effects of MCPG on hippocampal LTP, LTD, and depotentiation

1995 ◽  
Vol 74 (3) ◽  
pp. 1075-1082 ◽  
Author(s):  
D. K. Selig ◽  
H. K. Lee ◽  
M. F. Bear ◽  
R. C. Malenka
Keyword(s):  
Hippocampal Neurons ◽  
Metabotropic Glutamate Receptor ◽  
Low Frequency ◽  
Extracellular Recording ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Metabotropic Glutamate ◽  
Term Potentiation ◽  
Frequency Stimulation

1. We examined the effects of the metabotropic glutamate receptor (mGluR) antagonist alpha-methyl-4-carboxyphenylglycine (MCPG) on the induction of long-term potentiation (LTP) long-term depression (LTD), and depotentiation in CA1 hippocampal neurons using extracellular recording techniques. 2. MCPG (500 microM) strongly antagonized the presynaptic inhibitory action of the mGluR agonist 1-aminocyclopentane-(1S,3R)-dicarboxylic acid yet failed to block LTP induced with either tetanic stimulation (100 Hz, 1 s) or theta-burst stimulation. 3. To test the possibility that our failure to block LTP was due to prior activation of a "molecular switch" that in its "on" state obviates the need for mGluR activation to generate LTP, we gave repeated periods of prolonged low-frequency stimulation (LFS; 1 Hz, 10 min), a manipulation reported to turn the switch "off." Although this stimulation saturated LTD, subsequent application of MCPG still failed to block LTP. 4. MCPG did not block LFS-induced depotentiation in older slices (4-6 wk) or LFS-induced LTD in older, young (11-18 days), or neonatal (3-7 days) slices. 5. These results demonstrate that MCPG-sensitive mGluRs are not necessary for the induction of LTP, LTD, or depotentiation in hippocampal CA1 pyramidal cells. The possibility remains, however, that their activation may modify the threshold for the induction of these long-term plastic changes.

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