scholarly journals Transgenerational Rescue of a Genetic Defect in Long-Term Potentiation and Memory Formation by Juvenile Enrichment

2009 ◽  
Vol 29 (5) ◽  
pp. 1496-1502 ◽  
Author(s):  
J. A. Arai ◽  
S. Li ◽  
D. M. Hartley ◽  
L. A. Feig
Keyword(s):  
Genetic Defect ◽  
Long Term Potentiation ◽  
Memory Formation ◽  
Term Potentiation

scholarly journals Synaptic plasticity-dependent competition rule influences memory formation

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yire Jeong ◽  
Hye-Yeon Cho ◽  
Mujun Kim ◽  
Jung-Pyo Oh ◽  
Min Soo Kang ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Fear Conditioning ◽  
Long Term Potentiation ◽  
Memory Formation ◽  
Specific Pattern ◽  
Memory Encoding ◽  
Competition Rule ◽  
Term Potentiation ◽  
Input Activity

AbstractMemory is supported by a specific collection of neurons distributed in broad brain areas, an engram. Despite recent advances in identifying an engram, how the engram is created during memory formation remains elusive. To explore the relation between a specific pattern of input activity and memory allocation, here we target a sparse subset of neurons in the auditory cortex and thalamus. The synaptic inputs from these neurons to the lateral amygdala (LA) are not potentiated by fear conditioning. Using an optogenetic priming stimulus, we manipulate these synapses to be potentiated by the learning. In this condition, fear memory is preferentially encoded in the manipulated cell ensembles. This change, however, is abolished with optical long-term depression (LTD) delivered shortly after training. Conversely, delivering optical long-term potentiation (LTP) alone shortly after fear conditioning is sufficient to induce the preferential memory encoding. These results suggest a synaptic plasticity-dependent competition rule underlying memory formation.

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 The evidence for hippocampal long-term potentiation as a basis of memory for simple tasks

2008 ◽  
Vol 80 (1) ◽  
pp. 115-127 ◽  
Author(s):  
Iván Izquierdo ◽  
Martín Cammarota ◽  
Weber C. Da Silva ◽  
Lia R.M. Bevilaqua ◽  
Janine I. Rossato ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Brain Regions ◽  
Memory Formation ◽  
Long Term Memory ◽  
Ca1 Region ◽  
Term Potentiation ◽  
The One ◽  
Similar Task ◽  
Stimulation Of

Long-term potentiation (LTP) is the enhancement of postsynaptic responses for hours, days or weeks following the brief repetitive afferent stimulation of presynaptic afferents. It has been proposed many times over the last 30 years to be the basis of long-term memory. Several recent findings finally supported this hypothesis: a) memory formation of one-trial avoidance learning depends on a series of molecular steps in the CA1 region of the hippocampus almost identical to those of LTP in the same region; b)hippocampal LTP in this region accompanies memory formation of that task and of another similar task. However, CA1 LTP and the accompanying memory processes can be dissociated, and in addition plastic events in several other brain regions(amygdala, entorhinal cortex, parietal cortex) are also necessary for memory formation of the one-trial task, and perhaps of many others.

Learning and Memory

The Neuron ◽  
2015 ◽  
pp. 489-528
Author(s):  
Irwin B. Levitan ◽  
Leonard K. Kaczmarek
Keyword(s):  
Learning And Memory ◽  
Molecular Mechanisms ◽  
Long Term Potentiation ◽  
Memory Formation ◽  
Spike Timing ◽  
Cellular Mechanisms ◽  
Long Term Depression ◽  
Nervous Systems ◽  
Term Potentiation

Psychologists have described different kinds of learning and memory, and there is an ongoing search for the physical basis of these distinctions and for the cellular and molecular mechanisms responsible. Because of the complexity of most nervous systems, the search has focused to a large extent on animals with relatively simple nervous systems and on reduced preparations. Common themes have emerged, such as the requirement for signaling pathways linked to calcium and cyclic AMP, and the fact that pathways used in normal development continue to be used for plasticity in adults. At the same time, it is clear that there is an enormous diversity of cellular mechanisms that contribute to short-term and long-term phases of memory formation. These include long-term potentiation (LTP), long-term depression (LTD), spike-timing dependent plasticity, synaptic tagging, and synaptic scaling. Each type of synaptic connection has its own personality such that, in response to a particular pattern of stimulation, one synapse may increase its postsynaptic receptors while another may expand its presynaptic terminals.

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