De Novo Protein Synthesis of Syntaxin-1 and Dynamin-1 in Long-Term Memory Formation Requires CREB1 Gene Transcription in Lymnaea stagnalis

2010 ◽  
Vol 40 (5) ◽  
pp. 680-693 ◽  
Author(s):  
Cong-Hui Guo ◽  
Anthony Senzel ◽  
Kathy Li ◽  
Zhong-Ping Feng
2018 ◽  
Vol 342 ◽  
pp. 89-93 ◽  
Author(s):  
Kioko Guzmán-Ramos ◽  
Archana Venkataraman ◽  
Jean-Pascal Morin ◽  
Daniel Osorio-Gómez ◽  
Federico Bermúdez-Rattoni

2012 ◽  
Vol 215 (24) ◽  
pp. 4322-4329 ◽  
Author(s):  
M. L. Teskey ◽  
K. S. Lukowiak ◽  
H. Riaz ◽  
S. Dalesman ◽  
K. Lukowiak

2005 ◽  
Vol 21 (5) ◽  
pp. 1347-1358 ◽  
Author(s):  
Daniel Fulton ◽  
Ildiko Kemenes ◽  
Richard J. Andrew ◽  
Paul R. Benjamin

2011 ◽  
Vol 82 (2) ◽  
pp. 311-319 ◽  
Author(s):  
Sarah Dalesman ◽  
Simon D. Rundle ◽  
Ken Lukowiak

Author(s):  
Jacqunae L. Mays ◽  
Mauro Costa-Mattioli

The integrated stress response (ISR) is an evolutionarily conserved intracellular signaling network that responds to proteostasis defects and stress conditions by tuning protein synthesis rates. While it has been long recognized that long-term memory formation requires new protein synthesis, our understanding of the central translational control mechanisms that regulate memory formation has advanced vastly. Indeed, novel causal and convergent evidence across different species and model systems shows that the ISR serves as a universal regulator of long-term memory formation. This chapter discusses the evidence explaining how inhibition of the ISR enhances long-term memory formation while activation of the ISR prevents it. In addition, it highlights the role of the ISR in different forms of long-lasting synaptic plasticity in the brain. Finally, the chapter addresses how dysregulated ISR signaling contributes to the pathogenesis of a wide range of cognitive and neurodegenerative disorders and discusses the future prospects for therapeutically targeting the ISR for the treatment of cognitive disorders.


2002 ◽  
Vol 88 (4) ◽  
pp. 1584-1591 ◽  
Author(s):  
Andi Scheibenstock ◽  
Darin Krygier ◽  
Zara Haque ◽  
Naweed Syed ◽  
Ken Lukowiak

The cellular basis of long-term memory (LTM) storage is not completely known. We have developed a preparation where we are able to specify that a single identified neuron, Right Pedal Dorsal 1 (RPeD1), is a site of LTM formation of associative learning in the pond snail, Lymnaea stagnalis. We demonstrated this by ablating the soma of the neuron but leaving behind its functional primary neurite, as evidenced by electrophysiological and behavioral analyses. The soma-less RPeD1 neurite continues to be a necessary participant in the mediation of aerial respiratory behavior, associative learning, and intermediate-term memory (ITM); however, LTM cannot be formed. However, if RPeD1's soma is ablated after LTM consolidation has occurred, LTM can still be accessed. Thus the soma of RPeD1 is a site of LTM formation.


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