scholarly journals Critical Role of Endoplasmic Reticulum Stress in Chronic Intermittent Hypoxia-Induced Deficits in Synaptic Plasticity and Long-Term Memory

2015 ◽  
Vol 23 (9) ◽  
pp. 695-710 ◽  
Author(s):  
Lin-Hao Xu ◽  
Hui Xie ◽  
Zhi-Hui Shi ◽  
Li-Da Du ◽  
Yun-Kwok Wing ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Synaptic Plasticity ◽  
Endoplasmic Reticulum Stress ◽  
Intermittent Hypoxia ◽  
Critical Role ◽  
Chronic Intermittent Hypoxia ◽  
Long Term Memory ◽  
Term Memory

Role of atypical protein kinases in maintenance of long-term memory and synaptic plasticity

2017 ◽  
Vol 82 (3) ◽  
pp. 243-256 ◽  
Author(s):  
A. A. Borodinova ◽  
A. B. Zuzina ◽  
P. M. Balaban
Keyword(s):  
Synaptic Plasticity ◽  
Protein Kinases ◽  
Long Term Memory ◽  
Term Memory

scholarly journals Reading Memory Formation from the Eyes

2018 ◽  
Author(s):  
Anne Bergt ◽  
Anne E. Urai ◽  
Tobias H. Donner ◽  
Lars Schwabe
Keyword(s):  
Synaptic Plasticity ◽  
Memory Formation ◽  
Pupil Dilation ◽  
Long Term Memory ◽  
Term Memory ◽  
Pupil Response ◽  
Rapid Formation ◽  
The Brain

At any time, we are processing thousands of stimuli, but only few of them will be remembered hours or days later. Is there any way to predict which ones? Here, we show that the pupil response to ongoing stimuli, an indicator of physiological arousal, is a reliable predictor of long-term memory for these stimuli, over at least one day. Pupil dilation was tracked while participants performed visual and auditory encoding tasks. Memory was tested immediately after encoding and 24 hours later. Irrespective of the encoding modality, trial-by-trial variations in pupil dilation predicted which stimuli were recalled in the immediate and 24 hours-delayed tests. These results show that our eyes may provide a window into the formation of long-term memories. Furthermore, our findings underline the important role of central arousal systems in the rapid formation of memories in the brain, possibly by gating synaptic plasticity mechanisms.

scholarly journals Methamphetamine Inhibits Long-Term Memory Acquisition and Synaptic Plasticity by Evoking Endoplasmic Reticulum Stress

2021 ◽  
Vol 14 ◽  
Author(s):  
Guang Chen ◽  
Xiaoning Wei ◽  
Xiang Xu ◽  
Gang Yu ◽  
Zheng Yong ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Synaptic Plasticity ◽  
Er Stress ◽  
Memory Loss ◽  
Translation Initiation Factor ◽  
Long Term Memory ◽  
Term Memory ◽  
Expression Levels ◽  
Memory Acquisition

Methamphetamine (MA), an illicit drug abused worldwide, leads to cognitive impairment and memory loss. However, the detailed mechanisms of MA-induced neurologic impairment are still unclear. The present study aimed to investigate the mechanisms of MA-induced inhibition of memory acquisition from the perspective of endoplasmic reticulum (ER) stress. ER stress, caused by the accumulation of wrongly folded proteins in the ER, is important for new protein synthesis, which further influence the formation of long-term memory. A subacute MA poisoning model of mice was established and several behavioral experiments were performed, including elevated plus maze, Morris water maze, electro-stimulus Y-maze, and novel object recognition tasks. The present results suggested that 4 days exposure to MA induced significant memory loss. Whereas, this damage to memory formation could be protected when mice were pre-treated with ER stress inhibitor, tauroursodeoxycholic acid (TUDCA). The results of Western blotting showed that subacute exposure to MA increased the expression levels of ER stress marker proteins, such as binding immunoglobulin protein, phosphorylated eukaryotic translation initiation factor 2α, cyclic AMP-dependent transcription factor (ATF)-4, ATF-6, and CCAAT-enhancer binding protein homologous protein. Meanwhile, the enhanced expression levels of these proteins were reversed by TUDCA, indicating that MA administration induced memory loss by evoking ER stress in the hippocampus. We also found that MA inhibited the induction of long-term potentiation (LTP) in the hippocampus. Nevertheless, LTP could be induced when mice were pre-treated with TUDCA. In conclusion, MA inhibited long-term memory acquisition and synaptic plasticity via ER stress.

scholarly journals Dynamic Integrative Synaptic Plasticity Explains the Spacing Effect in the Transition from Short- to Long-Term Memory

2019 ◽  
Vol 31 (11) ◽  
pp. 2212-2251 ◽  
Author(s):  
Terry Elliott
Keyword(s):  
Synaptic Plasticity ◽  
Mapk Pathway ◽  
Spacing Effect ◽  
Long Term Memory ◽  
Pass Filter ◽  
Low Pass Filter ◽  
Term Memory ◽  
Low Pass

Repeated stimuli that are spaced apart in time promote the transition from short- to long-term memory, while massing repetitions together does not. Previously, we showed that a model of integrative synaptic plasticity, in which plasticity induction signals are integrated by a low-pass filter before plasticity is expressed, gives rise to a natural timescale at which to repeat stimuli, hinting at a partial account of this spacing effect. The account was only partial because the important role of neuromodulation was not considered. We now show that by extending the model to allow dynamic integrative synaptic plasticity, the model permits synapses to robustly discriminate between spaced and massed repetition protocols, suppressing the response to massed stimuli while maintaining that to spaced stimuli. This is achieved by dynamically coupling the filter decay rate to neuromodulatory signaling in a very simple model of the signaling cascades downstream from cAMP production. In particular, the model's parameters may be interpreted as corresponding to the duration and amplitude of the waves of activity in the MAPK pathway. We identify choices of parameters and repetition times for stimuli in this model that optimize the ability of synapses to discriminate between spaced and massed repetition protocols. The model is very robust to reasonable changes around these optimal parameters and times, but for large changes in parameters, the model predicts that massed and spaced stimuli cannot be distinguished or that the responses to both patterns are suppressed. A model of dynamic integrative synaptic plasticity therefore explains the spacing effect under normal conditions and also predicts its breakdown under abnormal conditions.

The role of PKMζ in the maintenance of long-term memory: a review

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Hamish Patel ◽  
Reza Zamani
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Long Term Potentiation ◽  
Global Memory ◽  
Long Term Memory ◽  
Compensatory Mechanism ◽  
Term Memory ◽  
Kinase C

Abstract Long-term memories are thought to be stored in neurones and synapses that undergo physical changes, such as long-term potentiation (LTP), and these changes can be maintained for long periods of time. A candidate enzyme for the maintenance of LTP is protein kinase M zeta (PKMζ), a constitutively active protein kinase C isoform that is elevated during LTP and long-term memory maintenance. This paper reviews the evidence and controversies surrounding the role of PKMζ in the maintenance of long-term memory. PKMζ maintains synaptic potentiation by preventing AMPA receptor endocytosis and promoting stabilisation of dendritic spine growth. Inhibition of PKMζ, with zeta-inhibitory peptide (ZIP), can reverse LTP and impair established long-term memories. However, a deficit of memory retrieval cannot be ruled out. Furthermore, ZIP, and in high enough doses the control peptide scrambled ZIP, was recently shown to be neurotoxic, which may explain some of the effects of ZIP on memory impairment. PKMζ knockout mice show normal learning and memory. However, this is likely due to compensation by protein-kinase C iota/lambda (PKCι/λ), which is normally responsible for induction of LTP. It is not clear how, or if, this compensatory mechanism is activated under normal conditions. Future research should utilise inducible PKMζ knockdown in adult rodents to investigate whether PKMζ maintains memory in specific parts of the brain, or if it represents a global memory maintenance molecule. These insights may inform future therapeutic targets for disorders of memory loss.

Sign in / Sign up

Export Citation Format

Share Document