Dynamics of Induction and Expression of Long-Term Synaptic Facilitation in<i>Aplysia</i>

Mauelshagen, Juliane; PARKER, G.; Carew, Thomas

doi:10.1523/jneurosci.16-22-07099.1996

Cited by 101 publications

(130 citation statements)

References 35 publications

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“…Single training trials lead to short-term sensitization lasting for hours and multiple spaced trials lead to long-term sensitization that last for days. 24 Formation of short term or long term memory is mirrored by short-term or long-term facilitation (increased neurotransmitter release) from sensory neurons that mediate touch onto motor neuron synapses that mediate a withdrawal response. 15,25 This facilitation of neurotransmitter release is mediated by shock-triggered serotonin that induces cAMP signaling and resultant PKA activation in presynaptic endings of sensory neurons.…”

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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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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“…A classical model of synaptic plasticity is facilitation of the sensorimotor synapse in Aplysia (30,109,154,155,227). In this model system, serotonin release onto the presynaptic terminal initiates intracellular cascades, increasing synaptic strength in multiple time domains.…”

Section: Changes In Synaptic Strengthmentioning

confidence: 99%

“…Important forms of synaptic plasticity are elicited preferentially by intermittent vs. sustained stimuli. For example, in Aplysia, serotonin-dependent LTF (154,155) and sustained PKA activation (227) are elicited by episodic serotonin exposures but not by serotonin exposures of equal total duration when applied in a "massed" or continuous pattern. Hippocampal LTP is most effectively induced by repeated tetanization (97).…”

Section: The Stimulus Paradigm Is a Key Determinant Of Plasticitymentioning

confidence: 99%

Invited Review: Neuroplasticity in respiratory motor control

Mitchell

Johnson

2003

Journal of Applied Physiology

354

313

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Although recent evidence demonstrates considerable neuroplasticity in the respiratory control system, a comprehensive conceptual framework is lacking. Our goals in this review are to define plasticity (and related neural properties) as it pertains to respiratory control and to discuss potential sites, mechanisms, and known categories of respiratory plasticity. Respiratory plasticity is defined as a persistent change in the neural control system based on prior experience. Plasticity may involve structural and/or functional alterations (most commonly both) and can arise from multiple cellular/synaptic mechanisms at different sites in the respiratory control system. Respiratory neuroplasticity is critically dependent on the establishment of necessary preconditions, the stimulus paradigm, the balance between opposing modulatory systems, age, gender, and genetics. Respiratory plasticity can be induced by hypoxia, hypercapnia, exercise, injury, stress, and pharmacological interventions or conditioning and occurs during development as well as in adults. Developmental plasticity is induced by experiences (e.g., altered respiratory gases) during sensitive developmental periods, thereby altering mature respiratory control. The same experience later in life has little or no effect. In adults, neuromodulation plays a prominent role in several forms of respiratory plasticity. For example, serotonergic modulation is thought to initiate and/or maintain respiratory plasticity following intermittent hypoxia, repeated hypercapnic exercise, spinal sensory denervation, spinal cord injury, and at least some conditioned reflexes. Considerable work is necessary before we fully appreciate the biological significance of respiratory plasticity, its underlying cellular/molecular and network mechanisms, and the potential to harness respiratory plasticity as a therapeutic tool.

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“…Recent studies have begun to define intermediate forms of facilitation (Sossin et al 1994;Ghirardi et al 1995;Mauelshagen et al 1996) and facilitation that persists 48 hr after a single series of stimulations (Zhang et al 1994. Treatments for establishing LTF without producing short-term facilitation have also been described (Emptage and Carew 1993).…”

Section: Molecular Changes In Ltf and Sensitizationmentioning

confidence: 99%

Identification of specific mRNAs affected by treatments producing long-term facilitation in Aplysia.

Zwartjes

West

Hattar³

et al. 1998

Learn. Mem.

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Neural correlates of long-term sensitization of defensive withdrawal reflexes in Aplysia occur in sensory neurons in the pleural ganglia and can be mimicked by exposure of these neurons to serotonin (5-HT). Studies using inhibitors indicate that transcription is necessary for production of long-term facilitation by 5-HT. Several mRNAs that change in response to 5-HT have been identified, but the molecular events responsible for long-term facilitation have not yet been fully described. To detect additional changes in mRNAs, we investigated the effects of 5-HT (1.5 hr) on levels of mRNA in pleural-pedal ganglia using in vitro translation. Four mRNAs were affected by 5-HT, three of which were identified as calmodulin (CaM), phosphoglycerate kinase (PGK), and a novel gene product (protein 3). Using RNase protection assays, we found that 5-HT increased all three mRNAs in the pleural sensory neurons. CaM and protein 3 mRNAs were also increased in the sensory neurons 4Corresponding author.by sensitization training. Furthermore, stimulation of peripheral nerves of pleural-pedal ganglia, an in vitro analog of sensitization training, increased the incorporation of labeled amino acids into CaM, PGK, and protein 3. These results indicate that increases in CaM, PGK, and protein 3 are part of the early response of sensory neurons to stimuli that produce long-term facilitation, and that CaM and protein 3 could have a role in the generation of long-term sensitization.

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Dynamics of Induction and Expression of Long-Term Synaptic Facilitation inAplysia

Cited by 101 publications

References 35 publications

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

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

Invited Review: Neuroplasticity in respiratory motor control

Identification of specific mRNAs affected by treatments producing long-term facilitation in Aplysia.

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