Late-associativity, synaptic tagging, and the role of dopamine during LTP and LTD

Sajikumar, Sreedharan; Frey, Julietta U.

doi:10.1016/j.nlm.2004.03.003

Cited by 321 publications

(388 citation statements)

References 54 publications

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“…These critical experiments were later independently replicated by Frey's (Sajikumar and Frey, 2004a) and Morris's (O'Carroll and Morris, 2004) groups, and by other labs working both in the mammalian hippocampus (Young and Nguyen, 2005) and in Aplysia neuronal cultures (Casadio et al, 1999). They arguably represent the strongest evidence supporting the STC model.…”

Section: Accepted Manuscriptmentioning

confidence: 89%

“…The STC model was originally described based on evidence obtained in hippocampal L-LTP and Aplysia LTF, however, synaptic capture has been later also observed in protein synthesis-dependent late long-term depression (L-LTD, Figure 2H) (Kauderer and Kandel, 2000;Navakkode et al, 2005;Sajikumar and Frey, 2004a;Sajikumar et al, 2005). As described for L-LTP, a strong low-frequency stimulation protocol (such as 900 bursts, consisting in 3 stimuli at 20Hz, delivered at 1 Hz) administered to a synaptic input induce a late phase of LTD that can be captured by a subthreshold low frequency stimulus delivered to a second synaptic input in the same population of neurons ( Figure 2I).…”

Section: Ltp and Ltd Tagsmentioning

confidence: 99%

“…The STC hypothesis revisited 16 Recent work by Sajikumar and colleagues has revealed another intriguing new feature of lateassociativity in the mammalian hipocampus (Sajikumar and Frey, 2004a). They found that the consolidation of either LTP or LTD (capture of LTP or LTD) was facilitated in response to the previous induction of the late phase of the opposite form of synaptic plasticity in a separate population of synapses in the same neurons ( Figure 2L), a paradoxical phenomenon they originally referred to as "cross-tagging" (Sajikumar and Frey, 2004a), although it has been later renamed as "cross-capture" by other authors (Govindarajan et al, 2006;Morris, 2006), a term we also consider more appropriate.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…They found that the consolidation of either LTP or LTD (capture of LTP or LTD) was facilitated in response to the previous induction of the late phase of the opposite form of synaptic plasticity in a separate population of synapses in the same neurons ( Figure 2L), a paradoxical phenomenon they originally referred to as "cross-tagging" (Sajikumar and Frey, 2004a), although it has been later renamed as "cross-capture" by other authors (Govindarajan et al, 2006;Morris, 2006), a term we also consider more appropriate. In this case, the situation seems to be radically different to that described in Aplysia cultured neurons, in which LTD overrides, instead of facilitate, LTF (Guan et al, 2002).…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…The hippocampus receives dopaminergic, noradrenergic and cholinergic inputs that can modulate LTP induction and consolidation (Frey et al, 1991;Frey et al, 1990;Gelinas and Nguyen, 2005;Hu et al, 2007), and play a role in synaptic capture of both L-LTD and L-LTP, likely by regulating the induction of PRPs and thereby priming the cells for synaptic capture (Navakkode et al, 2007;Sajikumar and Frey, 2004a). However, ascending monoaminergic fibers may also facilitate hippocampal LTP induction and LTP-dependent learning processes in a global manner during arousal and attention by suppressing the slow afterhyperpolarization (sAHP) and increasing intrinsic excitability…”

Section: Cell-wide Facilitation Modulation Of Intrinsic Excitabilitymentioning

confidence: 99%

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Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited 10 years later

Barco

Armentia

Alarcón

2008

Neuroscience & Biobehavioral Reviews

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Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited ten years later, Neuroscience and Biobehavioral Reviews (2008Reviews ( ), doi:10.1016Reviews ( /j.neubiorev.2008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting galley proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.A c c e p t e d m a n u s c r i p t A c c e p t e d m a n u s c r i p tThe STC hypothesis revisited 2 Abstract A decade ago, the synaptic tagging hypothesis was proposed to explain how newly synthesized plasticity products can be specifically targeted to active synapses. A growing number of studies have validated the seminal findings that gave rise to this model, as well as contributed to unveil and expand the range of mechanisms underlying late-associativity and neuronal computation.Here, we will review what it was learnt during this past decade regarding the cellular and molecular mechanisms underlying synaptic tagging and synaptic capture. The accumulated experimental evidence has widened the theoretical framework set by the synaptic tagging and capture (STC) model and introduced concepts that were originally considered part of alternative models for explaining synapse-specific LTP. As a result, we believe that the STC model, now improved and expanded with these new ideas and concepts, still represents the most compelling hypothesis to explain late-associativity in synapse-specific plasticity processes. We will also discuss the impact of this model in our view of the integrative capability of neurons and associative learning. wordsKeywords: synaptic plasticity; LTP; associative learning; neuronal computation; synaptic tagging; synaptic capture; metaplasticity A c c e p t e d m a n u s c r i p tThe STC hypothesis revisited 3 Contents

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Section: Accepted Manuscriptmentioning

confidence: 89%

Section: Ltp and Ltd Tagsmentioning

confidence: 99%

Section: Accepted Manuscriptmentioning

confidence: 99%

Section: Accepted Manuscriptmentioning

confidence: 99%

Section: Cell-wide Facilitation Modulation Of Intrinsic Excitabilitymentioning

confidence: 99%

See 3 more Smart Citations

Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited 10 years later

Barco

Armentia

Alarcón

2008

Neuroscience & Biobehavioral Reviews

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Learning Theories

Donahoe¹

2010

The Corsini Encyclopedia of Psychology

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A theory consists of a set of principles based on observations typically obtained under controlled laboratory conditions. The function of theory is to summarize in a concise fashion observations in a field of study and to enable predictions about future observations in that field. Learning theory is concerned with the variables that produce long‐lasting changes in individual behavior and the cumulative effects of those variables acting over time. Although based on laboratory research, often with animals, the principles are intended to apply to all behavior including the behavior of humans.

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Postsynaptic BDNF‐TrkB signaling in synapse maturation, plasticity, and disease

Yoshii

Constantine‐Paton

2010

Developmental Neurobiology

624

392

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Brain-derived neurotrophic factor (BDNF) is a prototypic neurotrophin that regulates diverse developmental events from the selection of neural progenitors to the terminal dendritic differentiation and connectivity of neurons. We focus here on activity-dependent synaptic regulation by BDNF and its receptor, full length TrkB. BDNF-TrkB signaling is involved in transcription, translation, and trafficking of proteins during various phases of synaptic development and has been implicated in several forms of synaptic plasticity. These functions are carried out by a combination of the three signaling cascades triggered when BDNF binds TrkB: The mitogen-activated protein kinase (MAPK), the phospholipase Cc (PLC PLCc), and the phosphatidylinositol 3-kinase (PI3K) pathways. MAPK and PI3K play crucial roles in both translation and/or trafficking of proteins induced by synaptic activity, whereas PLCc regulates intracellular Ca 2+ that can drive transcription via cyclic AMP and a protein kinase C. Conversely, the abnormal regulation of BDNF is implicated in various developmental and neurodegenerative diseases that perturb neural development and function. We will discuss the current state of understanding BDNF signaling in the context of synaptic development and plasticity with a focus on the postsynaptic cell and close with the evidence that basic mechanisms of BDNF function still need to be understood to effectively treat genetic disruptions of these pathways that cause devastating neurodevelopmental diseases. '

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Late-associativity, synaptic tagging, and the role of dopamine during LTP and LTD

Cited by 321 publications

References 54 publications

Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited 10 years later

Synapse-specific stabilization of plasticity processes: The synaptic tagging and capture hypothesis revisited 10 years later

Learning Theories

Postsynaptic BDNF‐TrkB signaling in synapse maturation, plasticity, and disease

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