MAP Kinase Translocates into the Nucleus of the Presynaptic Cell and Is Required for Long-Term Facilitation in Aplysia

Martin, Kelsey C.; Michael, Dan; Rose, Jim; Barad, Mark; Casadio, Andrea; Zhu, Huixiang; Kandel, Eric R.

doi:10.1016/s0896-6273(00)80330-x

Cited by 512 publications

(441 citation statements)

References 64 publications

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“…The Ras-controlled Raf-MEK-ERK protein kinase signaling cascade is known to play a critical role in the development of neuronal plasticity Sweatt, 1996, 1997;Martin et al, 1997) and long-term memory formation (Atkins et al, 1998;Orban et al, 1999;Adams and Sweatt, 2002). Changes in ERK signaling have also been associated with drug-dependent behavioral plasticity (Pierce et al, 1999;Valjent et al, 2000;Mazzucchelli et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Knockout of ERK1 Enhances Cocaine-Evoked Immediate Early Gene Expression and Behavioral Plasticity

Ferguson

Fasano

Yang

et al. 2006

Neuropsychopharmacol

110

100

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The ability of cocaine to produce lasting neural adaptations in mesocorticolimbic brain regions is thought to promote drug seeking and facilitate addiction in humans. The Ras-controlled Raf-MEK-ERK protein kinase signaling cascade has been implicated in the behavioral and neurobiological actions of cocaine in animals. However, these pharmacological studies have not been able to determine the specific role of the two predominant isoforms of ERK (ERK1 and ERK2) in these processes. We report here that deletion of the ERK1 isoform, which leads to increased ERK2 stimulus-dependent signaling, facilitates the development of cocaine-induced psychomotor sensitization and the acquisition of a cocaine conditioned place preference. Conversely, pharmacological blockade of ERK signaling attenuates the development of psychomotor sensitization to cocaine. Finally, cocaine-evoked gene expression in mesocorticolimbic brain regions is potentiated in ERK1-deficient mice. Thus, alterations in ERK signaling influence both the neurobiological impact of cocaine and its ability to produce enduring forms of drug experience-dependent behavioral plasticity. Our results suggest that enhanced ERK2 signaling following repeated drug exposure may facilitate the development of forms of cocaine-induced plasticity that contribute to addiction.

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Section: Discussionmentioning

confidence: 99%

Knockout of ERK1 Enhances Cocaine-Evoked Immediate Early Gene Expression and Behavioral Plasticity

Ferguson

Fasano

Yang

et al. 2006

Neuropsychopharmacol

110

100

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“…32 In the nucleus, through phosphorylation, the kinases turn on a transcriptional activator CREB1 (cAMP response element binding protein-1) while inactivating a transcriptional repressor CREB2. 30,33,34 This initiates a learning-associated transcriptional cascade of activity-dependent mRNAs whose translation is required for LTM.…”

Section: Rna Regulation Is Central To Long-term Memory Formationmentioning

confidence: 99%

“…This occurred along with the growth of new stable contacts sites at the 1X5HT-tagged synapse. 30,33,52 Summary of various 5 -HT stimulation protocols and associated synapse specific, cell wide or capture based LTF given in Table 1.…”

Section: Rna Regulation Is Central To Long-term Memory Formationmentioning

confidence: 99%

Long-term memory consolidation: The role of RNA-binding proteins with prion-like domains

Sudhakaran

Ramaswami

2016

RNA Biology

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Long-term and short-term memories differ primarily in the duration of their retention. At a molecular level, long-term memory (LTM) is distinguished from short-term memory (STM) by its requirement for new gene expression. In addition to transcription (nuclear gene expression) the translation of stored mRNAs is necessary for LTM formation. The mechanisms and functions for temporal and spatial regulation of mRNAs required for LTM is a major contemporary problem, of interest from molecular, cell biological, neurobiological and clinical perspectives. This review discusses primary evidence in support for translational regulatory events involved in LTM and a model in which different phases of translation underlie distinct phases of consolidation of memories. However, it focuses largely on mechanisms of memory persistence and the role of prion-like domains in this defining aspect of long-term memory. We consider primary evidence for the concept that Cytoplasmic Polyadenylation Element Binding (CPEB) protein enables the persistence of formed memories by transforming in prion-like manner from a soluble monomeric state to a self-perpetuating and persistent polymeric translationally active state required for maintaining persistent synaptic plasticity. We further discuss prion-like domains prevalent on several other RNA-binding proteins involved in neuronal translational control underlying LTM. Growing evidence indicates that such RNA regulatory proteins are components of mRNP (RiboNucleoProtein) granules. In these proteins, prion-like domains, being intrinsically disordered, could mediate weak transient interactions that allow the assembly of RNP granules, a source of silenced mRNAs whose translation is necessary for LTM. We consider the structural bases for RNA granules formation as well as functions of disordered domains and discuss how these complicate the interpretation of existing experimental data relevant to general mechanisms by which prion-domain containing RBPs function in synapse specific plasticity underlying LTM.

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“…However, recent data, obtained in Aplysia, actually suggests that phosphorylation of the repressor CREB2 reduces its repressing activity (Martin et al, 1997). An optimal stimulus frequency for transcription in such a gene network might still, however, be explainable in terms of two competing processes that have different sensitivity to stimuli and opposing effects on transcription.…”

Section: 1mentioning

confidence: 99%

Modeling Transcriptional Control in Gene Networks—Methods, Recent Results, and Future Directions

Smolen

Baxter

Byrne

2000

Bulletin of Mathematical Biology

280

161

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Mathematical models are useful for providing a framework for integrating data and gaining insights into the static and dynamic behavior of complex biological systems such as networks of interacting genes. We review the dynamic behaviors expected from model gene networks incorporating common biochemical motifs, and we compare current methods for modeling genetic networks. A common modeling technique, based on simply modeling genes as ON-OFF switches, is readily implemented and allows rapid numerical simulations. However, this method may predict dynamic solutions that do not correspond to those seen when systems are modeled with a more detailed method using ordinary differential equations. Until now, the majority of gene network modeling studies have focused on determining the types of dynamics that can be generated by common biochemical motifs such as feedback loops or protein oligomerization. For example, these elements can generate multiple stable states for gene product concentrations, state-dependent responses to stimuli, circadian rhythms and other oscillations, and optimal stimulus frequencies for maximal transcription. In the future, as new experimental techniques increase the ease of characterization of genetic networks, qualitative modeling will need to be supplanted by quantitative models for specific systems.

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MAP Kinase Translocates into the Nucleus of the Presynaptic Cell and Is Required for Long-Term Facilitation in Aplysia

Cited by 512 publications

References 64 publications

Knockout of ERK1 Enhances Cocaine-Evoked Immediate Early Gene Expression and Behavioral Plasticity

Knockout of ERK1 Enhances Cocaine-Evoked Immediate Early Gene Expression and Behavioral Plasticity

Long-term memory consolidation: The role of RNA-binding proteins with prion-like domains

Modeling Transcriptional Control in Gene Networks—Methods, Recent Results, and Future Directions

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