Blocking Memory Reconsolidation Reverses Memory-Associated Changes in Glutamate Receptor Expression

Rose, Jacqueline K.; Rankin, Catharine H.

doi:10.1523/jneurosci.2049-06.2006

Cited by 78 publications

(71 citation statements)

References 35 publications

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“…As would be expected for long-term memory, blocking protein synthesis during training (with heat shock) blocked consolidation of the memory (Beck and Rankin 1995). Long-term habituation was also sensitive to reconsolidation blockade-habituated worms given reminder taps followed by heat shock lost the memory of habituation training (Rose and Rankin 2006). These data suggest that long-term mechanosensory habituation shares features of long-term memory described in other organisms.…”

Section: Long-term Memorysupporting

confidence: 59%

An elegant mind: Learning and memory in Caenorhabditis elegans

Ardiel¹,

Rankin²

2010

Learn. Mem.

273

191

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This article reviews the literature on learning and memory in the soil-dwelling nematode Caenorhabditis elegans. Paradigms include nonassociative learning, associative learning, and imprinting, as worms have been shown to habituate to mechanical and chemical stimuli, as well as learn the smells, tastes, temperatures, and oxygen levels that predict aversive chemicals or the presence or absence of food. In each case, the neural circuit underlying the behavior has been at least partially described, and forward and reverse genetics are being used to elucidate the underlying cellular and molecular mechanisms. Several genes have been identified with no known role other than mediating behavior plasticity.Historically, it was believed that even if they were capable of learning, the nervous systems of invertebrates were too different to be instructive on human cognition. In the 1960s, Kandel and colleagues began studying learning in the marine mollusc Aplysia (Kandel and Tauc 1965). Using this system, they were able to relate behavioral plasticity to changes at specific synapses of identified neurons, and began a biochemical analysis of these neuronal changes, uncovering a role for cAMP, PKA, and CREB. In the 1970s, Benzer and colleagues began a genetic dissection of learning in the fruit fly Drosophila melanogaster (Quinn et al. 1974;Dudai et al. 1976). They established an associative learning assay (Quinn et al. 1974) and conducted a forward genetic screen, identifying the first learning mutant, dunce (Dudai et al. 1976). Since then, many genes have been cloned, and the biological basis of learning has proven to be highly conserved (Barco et al. 2006;Skoulakis and Grammenoudi 2006). Today there is no question as to the relevance of invertebrate research in the field of learning and memory.At about the same time that Kandel was beginning his work with Aplysia, Sydney Brenner chose Caenorhabditis elegans as the organism in which to study development and the nervous system (Brenner 1974). Today this transparent nematode is the world's best understood animal. It's small size ( 1 mm), short life cycle (,3 d), and ease of cultivation make it perfect for the laboratory, and its mode of reproduction is ideal for genetic analysis-selffertilizing hermaphrodites can be easily inbred or crossed with males. The genome has been mapped and sequenced, and there are thousands of mutants and RNAi constructs readily available for researchers. Furthermore, C. elegans has an invariant cell lineage and relatively simple morphology-959 cells make up the entire adult hermaphrodite (Sulston and Horvitz 1977;Sulston et al. 1983). Using serial section electron micrographs, White et al. (1986) were able to construct a neural wiring diagram of the hermaphrodite's 302 neurons. They found about 5000 chemical synapses, 600 gap junctions, and 2000 neuromuscular junctions, the location of which were fairly consistent between animals. With its invariant cell lineage and reproducible connectome, C. elegans was initially viewed as a genetically hardwired ...

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Section: Long-term Memorysupporting

confidence: 59%

An elegant mind: Learning and memory in Caenorhabditis elegans

Ardiel¹,

Rankin²

2010

Learn. Mem.

273

191

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“…In these amnesic animals, this also leads to the absence of ERK and its downstream transcription factors in the nucleus accumbens (see also Valjent et al 2006, who show a reduction in ERK and GluA1 phosphorylation using a similar procedure). Studying mechanisms of long-term habituation in Caenorhabditis elegans, Rose and Rankin (2006) showed that administering heat-shock or the non-N-methyl-D-aspartate (NMDA) glutamatergic antagonist, DMQX, after reactivation of a consolidated memory dramatically returns expression of aamino-3-hydroxy-5-methyl-4-isoxazolepropionic (AMPA) receptors in the mechanosensory neuron to a level typical for naïve animals (Rose and Rankin 2006). Importantly, the reconsolidation effects in all of these studies were contingent on memory reactivation-in the absence of a reminder the amnesic treatments were ineffective.…”

Section: Reconsolidation and The Dynamic Nature Of Memorymentioning

confidence: 99%

Reconsolidation and the Dynamic Nature of Memory

Nader

2015

Cold Spring Harb Perspect Biol

147

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Memory reconsolidation is the process in which reactivated long-term memory (LTM) becomes transiently sensitive to amnesic agents that are effective at consolidation. The phenomenon was first described more than 50 years ago but did not fit the dominant paradigm that posited that consolidation takes place only once per LTM item. Research on reconsolidation was revitalized only more than a decade ago with the demonstration of reconsolidation in a well-defined behavioral protocol (auditory fear conditioning in the rat) subserved by an identified brain circuit (basolateral amygdala). Since then, reconsolidation has been shown in many studies over a range of species, tasks, and amnesic agents, and cellular and molecular correlates of reconsolidation have also been identified. In this review, I will first define the evidence on which reconsolidation is based, and proceed to discuss some of the conceptual issues facing the field in determining when reconsolidation does and does not occur. Last, I will refer to the potential clinical implications of reconsolidation.

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“…Pharmacological blockade of non-NMDA (N-methyl-D-aspartic acid) type glutamate receptors with 6, 7-dinitroquinoxaline-2,3-dione (DNQX) during reminder also eliminated the 48-h retention. Furthermore, the expression level of specific glutamate receptor subunit (GLR-1) decreased significantly in trained animals compared with untrained controls, and the effect of training on GLR-1 levels was reversed if the trained animals were given a reminder immediately followed by heat shock [24] . Therefore, both the behavioral expression of long-term memory for habituation and a cellular correlation of that memory can be altered after retrieval in C. elegans [24] .…”

Section: Intermediate Memory For Habituationmentioning

confidence: 99%

“…Therefore, both the behavioral expression of long-term memory for habituation and a cellular correlation of that memory can be altered after retrieval in C. elegans [24] . In addition, similar mechanisms are involved in the control of memory consolidation and memory reconsolidation, since conditions that impair memory consolidation similarly disrupt memory reconsolidation [24] . These findings also confirm the previous observation that GLR-1 cluster density was closely correlated with the expression of memory for habituation.…”

Section: Intermediate Memory For Habituationmentioning

confidence: 99%

“…Furthermore, the expression level of specific glutamate receptor subunit (GLR-1) decreased significantly in trained animals compared with untrained controls, and the effect of training on GLR-1 levels was reversed if the trained animals were given a reminder immediately followed by heat shock [24] . Therefore, both the behavioral expression of long-term memory for habituation and a cellular correlation of that memory can be altered after retrieval in C. elegans [24] . In addition, similar mechanisms are involved in the control of memory consolidation and memory reconsolidation, since conditions that impair memory consolidation similarly disrupt memory reconsolidation [24] .…”

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confidence: 99%

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Molecular control of memory in nematode Caenorhabditis elegans

Wang

2008

Neurosci. Bull.

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·Minireview·Memory, one of the important properties of central nerve system (CNS), is defined as encoding, storage and retrieval of learned inputs. However, many complex processes of memory still need further scientific explanations. Invertebrate animals have been already widely accepted as successful organisms for the study of neuroscience, and many important discoveries on behavioral cognitive science were made in the model invertebrate animals [1,2] . Model invertebrate organisms such as Caenorhabditis elegans and Drosophila melanogaster have provided powerful genetic approaches to a series of central questions concerning neural development, learning and memory, and the cellular and molecular substrates of behaviors [3][4] . In this review, we will discuss the recent progress on the molecular control of memory based on the studies of model organism C. elegans, via different paradigms in which diverse environmental clues are involved. C. elegans has become an ideal organism model to unravel the complex processes of learning and memory [5] . Besides its extensively anatomical knowledge, the neural circuit of the worm can be analyzed by the technique of laser ablation for identified neurons. Its entire genome has been mapped and sequenced, which allow us to use the methods of systematic forward or reverse genetic screen to elucidate the molecular mechanisms of memory. Especially, C. elegans displays simple forms of memory, such as thermotaxis, chemotaxis and mechanotransdution [5] . Memory for thermosensationC. elegans depends on environmental temperature to sense and search food. Therefore thermotaxis may be the most powerful behavioral paradigm for elucidating the memory mechanism underlying this behavioral plasticity. That model gives an association between the temperature encoded into memory and the nutritional state, and the temperature-food association can be kept for a long period [6] . This thermosensory system exhibits properties of exquisite temperature sensitivity [storage of the thermotactic set-point (T s )], longterm plasticity (comparison of current temperature with the T s ), and the ability to transform thermosensory input into different patterns of motor neurons (measurement of thermal gradients during movement). In brief, the animals adjust a stored set-point of thermotactic memory to their cultivation temperature (T cult ) and the AFD (a sensory neuron)-AIY (an interneuron, the major postsynaptic partner of AFD)-AIZ (an interneuron, the major postsynaptic partner of AIY) neuron circuit: the AFD and AIY neurons specify the thermophilic components of the circuit, driving movement to higher temperatures in a thermal gradient; the AIY and AIZ neurons specify the cryophilic components of the circuit, driving movement to lower temperatures in a thermal gradient [7] . The time-course assay of thermotaxis suggested that a new temperature encoding is a relative long process, and which appears to be independent of cultivation temperature [6] . In addition, starvation can accelerate the memory formation...

show abstract

Blocking Memory Reconsolidation Reverses Memory-Associated Changes in Glutamate Receptor Expression

Cited by 78 publications

References 35 publications

An elegant mind: Learning and memory in Caenorhabditis elegans

An elegant mind: Learning and memory in Caenorhabditis elegans

Reconsolidation and the Dynamic Nature of Memory

Molecular control of memory in nematode Caenorhabditis elegans

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