scholarly journals Synaptic memory requires CaMKII

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Wucheng Tao ◽  
Joel Lee ◽  
Xiumin Chen ◽  
Javier Díaz-Alonso ◽  
Jing Zhou ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Learning And Memory ◽  
Long Term Potentiation ◽  
Cellular Model ◽  
Term Potentiation

Long-term potentiation (LTP) is arguably the most compelling cellular model for learning and memory. While the mechanisms underlying the induction of LTP ('learning') are well understood, the maintenance of LTP ('memory') has remained contentious over the last 20 years. Here, we find that CaMKII contributes to synaptic transmission and is required LTP maintenance. Acute inhibition of CaMKII erases LTP and transient inhibition of CaMKII enhances subsequent LTP. These findings strongly support the role of CaMKII as a molecular storage devise.

scholarly journals Learning-induced modulation of the effect of neuroglial transmission on synaptic plasticity

2018 ◽  
Vol 119 (6) ◽  
pp. 2373-2379 ◽  
Author(s):  
Luna Jammal ◽  
Ben Whalley ◽  
Edi Barkai
Keyword(s):  
Synaptic Transmission ◽  
Gap Junctions ◽  
Piriform Cortex ◽  
Rule Learning ◽  
Long Term Potentiation ◽  
Synaptic Inhibition ◽  
Term Potentiation ◽  
Term Maintenance

Training rats in a complex olfactory discrimination task results in acquisition of “rule learning” (learning how to learn), a term describing the capability to perform the task superbly. Such rule learning results in strengthening of both excitatory and inhibitory synaptic connections between neurons in the piriform cortex. Moreover, intrinsic excitability is also enhanced throughout the pyramidal neuron population. Surprisingly, the cortical network retains its stability under these long-term modifications. In particular, the susceptibility for long-term potentiation (LTP) induction, while decreased for a short time window, returns to almost its pretraining value, although significant strengthening of AMPA receptor-mediated glutamatergic transmission remains. Such network balance is essential for maintaining the single-cell modifications that underlie long-term memory while preventing hyperexcitability that would result in runaway synaptic activity. However, the mechanisms underlying the long-term maintenance of such balance have yet to be described. In this study, we explored the role of astrocyte-mediated gliotransmission in long-term maintenance of learning-induced modifications in susceptibility for LTP induction and control of the strength of synaptic inhibition. We show that blocking connexin 43 hemichannels, which form gap junctions between astrocytes, decreases significantly the ability to induce LTP by stimulating the excitatory connections between piriform cortex pyramidal neurons after learning only. In parallel, spontaneous miniature inhibitory postsynaptic current amplitude is reduced in neurons from trained rats only, to the level of prelearning. Thus gliotransmission has a key role in maintaining learning-induced cortical stability by a wide-ranged control on synaptic transmission and plasticity. NEW & NOTEWORTHY We explore the role of astrocyte-mediated gliotransmission in maintenance of olfactory discrimination learning-induced modifications. We show that blocking gap junctions between astrocytes decreases significantly the ability to induce long-term potentiation in the piriform cortex after learning only. In parallel, synaptic inhibition is reduced in neurons from trained rats only, to the level of prelearning. Thus gliotransmission has a key role in maintaining learning-induced cortical stability by a wide-ranged control on synaptic transmission and plasticity.

Cholinergic modulation of hippocampal long-term potentiation in chronic cerebral hypoperfused rats

2018 ◽  
Vol 1 (1) ◽  
pp. 42-57 ◽  
Author(s):  
Nor Fasihah Azam ◽  
Ryan Andrew Stanyard ◽  
Noorul Hamizah Mat ◽  
Zurina Hassan
Keyword(s):  
Synaptic Transmission ◽  
Rat Model ◽  
Neuronal Loss ◽  
Long Term Potentiation ◽  
Cerebral Hypoperfusion ◽  
Vessel Occlusion ◽  
Term Potentiation ◽  
Significant Impairment

Vascular dementia (VaD) is one of the most common types of dementia in Alzheimer’s disease (AD). Two-vessel occlusion (2VO), also known as permanent bilateral occlusion of the common carotid arteries, induces chronic cerebral hypoperfusion (CCH) in rats, resulting in neuronal loss and inflammation (particularly in the cortex and hippocampus).  The 2VO rat model has been widely used to represent VaD conditions similar to those seen in humans. Synaptic plasticity or long-term potentiation (LTP) is one of the most important neurochemical foundations in learning and memory, deficits of which occur as a result of VaD. The aim of this study is to evaluate the role of cholinergic transmission in LTP impairment of CCH rat model. There is a significant impairment of LTP following the induction of 2VO surgery (p < .05). Treatment with oxotremorine and tacrine cause significant enhancement of LTP and potentiation levels (p < .05). There are also significant effects of paired-pulse facilitations when treated with cholinergic agonists and baseline synaptic transmission with increasing stimulation intensity (p < .0001). AChE activity was only found to increase significantly in the hippocampal region (p < .05). The role of cholinergic neurotransmission has been clearly demonstrated in LTP impairment of the CCH rat model. Augmentation of synaptic transmission was clearly observed in this model via changes of basal synaptic transmission and neurotransmitter release presynaptically.

The role of Ca2+ channels in hippocampal mossy fiber synaptic transmission and long-term potentiation

Neuron ◽  
1994 ◽  
Vol 12 (2) ◽  
pp. 261-269 ◽  
Author(s):  
Pablo E. Castillo ◽  
Marc G. Weisskopf ◽  
Roger A. Nicoll
Keyword(s):  
Synaptic Transmission ◽  
Mossy Fiber ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Ca2 Channels

Pleiotrophin inhibits hippocampal long-term potentiation: A role of pleiotrophin in learning and memory

2009 ◽  
Vol 27 (3) ◽  
pp. 189-194 ◽  
Author(s):  
Nuria del Olmo ◽  
Esther Gramage ◽  
Luis F. Alguacil ◽  
Pablo Pérez-Pinera ◽  
Thomas F. Deuel ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Long Term Potentiation ◽  
Term Potentiation

scholarly journals Chondroitin 6-sulphate is required for neuroplasticity and memory in ageing

2021 ◽  
Author(s):  
Sujeong Yang ◽  
Sylvain Gigout ◽  
Angelo Molinaro ◽  
Yuko Naito-Matsui ◽  
Sam Hilton ◽  
...  
Keyword(s):  
Chondroitin Sulphate ◽  
Memory Loss ◽  
Memory Deficits ◽  
Long Term Potentiation ◽  
Aged Mice ◽  
Age Related ◽  
Term Potentiation ◽  
Early Memory

AbstractPerineuronal nets (PNNs) are chondroitin sulphate proteoglycan-containing structures on the neuronal surface that have been implicated in the control of neuroplasticity and memory. Age-related reduction of chondroitin 6-sulphates (C6S) leads to PNNs becoming more inhibitory. Here, we investigated whether manipulation of the chondroitin sulphate (CS) composition of the PNNs could restore neuroplasticity and alleviate memory deficits in aged mice. We first confirmed that aged mice (20-months) showed memory and plasticity deficits. They were able to retain or regain their cognitive ability when CSs were digested or PNNs were attenuated. We then explored the role of C6S in memory and neuroplasticity. Transgenic deletion of chondroitin 6-sulfotransferase (chst3) led to a reduction of permissive C6S, simulating aged brains. These animals showed very early memory loss at 11 weeks old. Importantly, restoring C6S levels in aged animals rescued the memory deficits and restored cortical long-term potentiation, suggesting a strategy to improve age-related memory impairment.

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