scholarly journals Compartmentalized PKA signaling events are required for synaptic tagging and capture during hippocampal late-phase long-term potentiation

2006 ◽  
Vol 85 (7) ◽  
pp. 635-642 ◽  
Author(s):  
Ted Huang ◽  
Conor B. McDonough ◽  
Ted Abel
Keyword(s):  
Late Phase ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Signaling Events ◽  
Synaptic Tagging And Capture

scholarly journals The Role of Extracellular Regulated Kinases I/II in Late-Phase Long-Term Potentiation

2002 ◽  
Vol 22 (13) ◽  
pp. 5432-5441 ◽  
Author(s):  
Kobi Rosenblum ◽  
Marie Futter ◽  
Karen Voss ◽  
Muriel Erent ◽  
Paul A. Skehel ◽  
...  
Keyword(s):  
Late Phase ◽  
Long Term Potentiation ◽  
Term Potentiation

scholarly journals Fructose 1,6-Bisphosphatase 2 Plays a Crucial Role in the Induction and Maintenance of Long-Term Potentiation

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1375 ◽  
Author(s):  
Przemysław Duda ◽  
Tomasz Wójtowicz ◽  
Jakub Janczara ◽  
Daniel Krowarsch ◽  
Aleksandra Czyrek ◽  
...  
Keyword(s):  
Molecular Basis ◽  
Late Phase ◽  
Long Term Potentiation ◽  
Memory Formation ◽  
Lactate Shuttle ◽  
Term Potentiation ◽  
Fructose 1,6 Bisphosphatase ◽  
Nadh Ratio ◽  
Simultaneous Inhibition

Long-term potentiation (LTP) is a molecular basis of memory formation. Here, we demonstrate that LTP critically depends on fructose 1,6-bisphosphatase 2 (Fbp2)—a glyconeogenic enzyme and moonlighting protein protecting mitochondria against stress. We show that LTP induction regulates Fbp2 association with neuronal mitochondria and Camk2 and that the Fbp2–Camk2 interaction correlates with Camk2 autophosphorylation. Silencing of Fbp2 expression or simultaneous inhibition and tetramerization of the enzyme with a synthetic effector mimicking the action of physiological inhibitors (NAD+ and AMP) abolishes Camk2 autoactivation and blocks formation of the early phase of LTP and expression of the late phase LTP markers. Astrocyte-derived lactate reduces NAD+/NADH ratio in neurons and thus diminishes the pool of tetrameric and increases the fraction of dimeric Fbp2. We therefore hypothesize that this NAD+-level-dependent increase of the Fbp2 dimer/tetramer ratio might be a crucial mechanism in which astrocyte–neuron lactate shuttle stimulates LTP formation.

scholarly journals Long-Term Potentiation and Memory

2004 ◽  
Vol 84 (1) ◽  
pp. 87-136 ◽  
Author(s):  
M. A. LYNCH
Keyword(s):  
Animal Models ◽  
Cell Signaling ◽  
Spatial Learning ◽  
Gene Knockout ◽  
Transgenic Animals ◽  
Long Term Potentiation ◽  
Afferent Pathways ◽  
Term Potentiation ◽  
Signaling Events

Lynch, MA. Long-Term Potentiation and Memory. Physiol Rev 84: 87–136, 2004; 10.1152/physrev.00014.2003.—One of the most significant challenges in neuroscience is to identify the cellular and molecular processes that underlie learning and memory formation. The past decade has seen remarkable progress in understanding changes that accompany certain forms of acquisition and recall, particularly those forms which require activation of afferent pathways in the hippocampus. This progress can be attributed to a number of factors including well-characterized animal models, well-defined probes for analysis of cell signaling events and changes in gene transcription, and technology which has allowed gene knockout and overexpression in cells and animals. Of the several animal models used in identifying the changes which accompany plasticity in synaptic connections, long-term potentiation (LTP) has received most attention, and although it is not yet clear whether the changes that underlie maintenance of LTP also underlie memory consolidation, significant advances have been made in understanding cell signaling events that contribute to this form of synaptic plasticity. In this review, emphasis is focused on analysis of changes that occur after learning, especially spatial learning, and LTP and the value of assessing these changes in parallel is discussed. The effect of different stressors on spatial learning/memory and LTP is emphasized, and the review concludes with a brief analysis of the contribution of studies, in which transgenic animals were used, to the literature on memory/learning and LTP.

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