Different Mechanisms and Multiple Stages of LTP

Matthies, H; Frey, Uwe; Reymann, Klaus G.; Krug, Manfred; Jork, R.; Schroeder, Helmut

doi:10.1007/978-1-4684-5769-8_39

Cited by 114 publications

(40 citation statements)

References 30 publications

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“…Classical LTP in the CA1 region of the hippocampus (E-LTP) persists for only a few hours and is independent of new protein synthesis. In contrast, longlasting LTP in the CA1 (L-LTP), which is produced by multiple trains of high-frequency stimuli, lasts for hours or even days and requires de novo transcription and protein synthesis (Grecksch and Matthies, 1980;Mathies et al, 1990;Huang et al, 1994;Nguyen et al, 1994). LTP may be a useful model for studying molecular mechanisms that contribute to learning and memory and to experience-dependent synaptic plasticity in the visual cortex (Grant et al, 1992;Silva et al, 1992;Kirkwood et al, 1995;Wu et al, 1995).…”

Section: Abstract: Transfection; Neurons; Transcription C-fos; Glutmentioning

confidence: 99%

Calcium Influx via the NMDA Receptor Induces Immediate Early Gene Transcription by a MAP Kinase/ERK-Dependent Mechanism

et al. 1996

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The regulation of gene expression by neurotransmitters is likely to play a key role in neuroplasticity both during development and in the adult animal. Therefore, it is important to determine the mechanisms of neuronal gene regulation to understand fully the mechanisms of learning, memory, and other long-term adaptive changes in neurons. The neurotransmitter glutamate stimulates rapid and transient induction of many genes, including the c-fos proto-oncogene. The c-fos promoter contains several critical regulatory elements, including the serum response element (SRE), that mediate glutamate-induced transcription in neurons; however, the mechanism by which the SRE functions in neurons has not been defined. In this study, we sought to identify transcription factors that mediate glutamate induction of transcription through the SRE in cortical neurons and to elucidate the mechanism(s) of transcriptional activation by these factors. To facilitate this analysis, we developed an improved calcium phosphate coprecipitation procedure to transiently introduce DNA into primary neurons, both efficiently and consistently. Using this protocol, we demonstrate that the transcription factors serum response factor (SRF) and Elk-1 can mediate glutamate induction of transcription through the SRE in cortical neurons. There are at least two distinct pathways by which glutamate signals through the SRE: an SRF-dependent pathway that can operate in the absence of Elk and an Elk-dependent pathway. Activation of the Elkdependent pathway of transcription seems to require phosphorylation of Elk-1 by extracellular signal-regulated kinases (ERKs), providing evidence for a physiological function of ERKs in glutamate signaling in neurons. Taken together, these findings suggest that SRF, Elk, and ERKs may have important roles in neuroplasticity.

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Section: Abstract: Transfection; Neurons; Transcription C-fos; Glutmentioning

confidence: 99%

Calcium Influx via the NMDA Receptor Induces Immediate Early Gene Transcription by a MAP Kinase/ERK-Dependent Mechanism

et al. 1996

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“…Currently, there are only two cellular phenomena which could underlie such prolonged changes called long-term potentiation (LTP) and long-term depression (LTD) (Matthies et al, 1990;Bear and Malenka, 1994;Frey and Frey, 2008). Both, LTP and LTD show distinct temporal stages such as a protein synthesis-independent early phase (early-LTP, early-LTD) and a protein synthesis-dependent late phase (late-LTP, late-LTD).…”

Section: Introductionmentioning

confidence: 99%

Interfering with the Actin Network and Its Effect on Long-Term Potentiation and Synaptic Tagging in Hippocampal CA1 Neurons in SlicesIn Vitro

Ramachandran

Frey²

2009

J. Neurosci.

117

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Long-term potentiation (LTP) is a cellular correlate for memory formation, which requires the dynamic changes of the actin cytoskeleton. As shown by others, the polymerization of the actin network is important for early stages of LTP. Here, we investigated the role of actin dynamics in synaptic tagging and particularly in the induction of protein synthesis-dependent late-LTP in the CA1 region in hippocampal slices in vitro. We found that the inhibition of actin polymerization affects protein synthesis-independent early-LTP, prevents late-LTP, and interferes with synaptic tagging in apical dendrites of hippocampal CA1. The transformation of early-LTP into late-LTP was blocked by the application of the structurally different actin polymerization inhibitors latrunculin A or cytochalasin D. We suggest that the actin network is required for early "housekeeping" processes to induce and maintain early-LTP. Furthermore, inhibition of actin dynamics negatively interacts with the setting of the synaptic tagging complex. We propose actin as a further tag-specific molecule in apical CA1 dendrites where it is directly involved in the tagging/capturing machinery. Consequently, inhibition of the actin network prevents the interaction of tagging complexes with plasticity-related proteins. This results in the prevention of late-LTP by inhibition of the actin network during LTP induction.

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“…However, distinct patterns of lowfrequency stimulation (LFS) can result in a long-term depression (LTD) of synaptic efficacy (Mulkey and Malenka, 1992;Bear and Malenka, 1994;Linden and Connor, 1995;Sajikumar and Frey, 2003). It has been reported that late LTP as well as late LTD in the hippocampal CA1 region from adult rats require the coactivation of the NMDA receptor (NMDAR), as well as dopaminergic D 1 and D 5 receptors and protein synthesis (Frey et al, 1988(Frey et al, , 1991a(Frey et al, ,b, 1993Matthies et al, 1990;Dudek and Bear, 1992;Huang and Kandel, 1995;Manahan-Vaughan, 2000;Frey, 2003, 2004). The activation of the cAMP/cAMPdependent protein kinase (PKA) pathway through the synergistic action of NMDAR and dopaminergic D 1 and D 5 receptor activation is crucial for the development of the protein synthesisdependent late LTP as well as late LTD in CA1 neurons from adult rats (Frey et al, , 1991b(Frey et al, , 1993Matthies et al, 1990;Matthies and Reymann, 1993;Huang and Kandel 1995;Abel et al, 1997;Morozov et al, 2003;Nguyen and Woo, 2003;Fischer et al, 2004;Sajikumar and Frey, 2004).…”

Section: Introductionmentioning

confidence: 99%

“…It has been reported that late LTP as well as late LTD in the hippocampal CA1 region from adult rats require the coactivation of the NMDA receptor (NMDAR), as well as dopaminergic D 1 and D 5 receptors and protein synthesis (Frey et al, 1988(Frey et al, , 1991a(Frey et al, ,b, 1993Matthies et al, 1990;Dudek and Bear, 1992;Huang and Kandel, 1995;Manahan-Vaughan, 2000;Frey, 2003, 2004). The activation of the cAMP/cAMPdependent protein kinase (PKA) pathway through the synergistic action of NMDAR and dopaminergic D 1 and D 5 receptor activation is crucial for the development of the protein synthesisdependent late LTP as well as late LTD in CA1 neurons from adult rats (Frey et al, , 1991b(Frey et al, , 1993Matthies et al, 1990;Matthies and Reymann, 1993;Huang and Kandel 1995;Abel et al, 1997;Morozov et al, 2003;Nguyen and Woo, 2003;Fischer et al, 2004;Sajikumar and Frey, 2004). Furthermore, LTP as well as LTD are characterized by late-associative properties involving processes of "synaptic tagging" (Frey andMorris, 1997, 1998;Kauderer and Kandel, 2000;Navakkode et al, 2004) and "synaptic cross-tagging" Sajikumar et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Mitogen-Activated Protein Kinase-Mediated Reinforcement of Hippocampal Early Long-Term Depression by the Type IV-Specific Phosphodiesterase Inhibitor Rolipram and Its Effect on Synaptic Tagging

Navakkode¹,

Sajikumar²,

Frey³

2005

J. Neurosci.

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Different Mechanisms and Multiple Stages of LTP

Cited by 114 publications

References 30 publications

Calcium Influx via the NMDA Receptor Induces Immediate Early Gene Transcription by a MAP Kinase/ERK-Dependent Mechanism

Calcium Influx via the NMDA Receptor Induces Immediate Early Gene Transcription by a MAP Kinase/ERK-Dependent Mechanism

Interfering with the Actin Network and Its Effect on Long-Term Potentiation and Synaptic Tagging in Hippocampal CA1 Neurons in SlicesIn Vitro

Mitogen-Activated Protein Kinase-Mediated Reinforcement of Hippocampal Early Long-Term Depression by the Type IV-Specific Phosphodiesterase Inhibitor Rolipram and Its Effect on Synaptic Tagging

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