scholarly journals Prolonged Systemic Inflammation Alters Muscarinic Long-Term Potentiation (mLTP) in the Hippocampus

2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Efrat Shavit-Stein ◽  
Amir Dori ◽  
Marina Ben Shimon ◽  
Shany Guly Gofrit ◽  
Nicola Maggio
Keyword(s):  
Cognitive Impairment ◽  
Systemic Inflammation ◽  
Long Term Potentiation ◽  
Short Exposure ◽  
Short Term ◽  
Cholinergic Dysfunction ◽  
Term Potentiation ◽  
Hippocampal Synapses ◽  
The Brain

The cholinergic system plays a fundamental role in learning and memory. Pharmacological activation of the muscarinic receptor M1R potentiates NMDA receptor activity and induces short-term potentiation at the synapses called muscarinic LTP, mLTP. Dysfunction of cholinergic transmission has been detected in the settings of cognitive impairment and dementia. Systemic inflammation as well as neuroinflammation has been shown to profoundly alter synaptic transmission and LTP. Indeed, intervention which is aimed at reducing neuroinflammatory changes in the brain has been associated with an improvement in cognitive functions. While cognitive impairment caused either by cholinergic dysfunction and/or by systemic inflammation suggests a possible connection between the two, so far whether systemic inflammation affects mLTP has not been extensively studied. In the present work, we explored whether an acute versus persistent systemic inflammation induced by LPS injections would differently affect the ability of hippocampal synapses to undergo mLTP. Interestingly, while a short exposure to LPS resulted in a transient deficit in mLTP expression, a longer exposure persistently impaired mLTP. We believe that these findings may be involved in cognitive dysfunctions following sepsis and possibly neuroinflammatory processes.

scholarly journals Neuraminidase Inhibition Primes Short-Term Depression and Suppresses Long-Term Potentiation of Synaptic Transmission in the Rat Hippocampus

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Alina Savotchenko ◽  
Arthur Romanov ◽  
Dmytro Isaev ◽  
Oleksandr Maximyuk ◽  
Vadym Sydorenko ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Synaptic Plasticity ◽  
Science Studies ◽  
Hippocampal Slices ◽  
Control Level ◽  
Specific Inhibitor ◽  
Long Term Potentiation ◽  
Short Term ◽  
Term Potentiation

Neuraminidase (NEU) is a key enzyme that cleaves negatively charged sialic acid residues from membrane proteins and lipids. Clinical and basic science studies have shown that an imbalance in NEU metabolism or changes in NEU activity due to various pathological conditions parallel with behavior and cognitive impairment. It has been suggested that the decreases of NEU activity could cause serious neurological consequences. However, there is a lack of direct evidences that modulation of endogenous NEU activity can impair neuronal function. Using combined rat entorhinal cortex/hippocampal slices and a specific inhibitor of NEU, 2-deoxy-2,3-dehydro-N-acetylneuraminic acid (NADNA), we examined the effect of downregulation of NEU activity on different forms of synaptic plasticity in the hippocampal CA3-to-CA1 network. We show that NEU inhibition results in a significant decrease in long-term potentiation (LTP) and an increase in short-term depression. Synaptic depotentiation restores LTP in NADNA-pretreated slices to the control level. These data suggest that short-term NEU inhibition produces the LTP-like effect on neuronal network, which results in damping of further LTP induction. Our findings demonstrate that downregulation of NEU activity could have a major impact on synaptic plasticity and provide a new insight into the cellular mechanism underlying behavioral and cognitive impairment associated with abnormal metabolism of NEU.

scholarly journals Multiplexed neurochemical transmission emulated using a dual-excitatory synaptic transistor

2021 ◽  
Vol 5 (1) ◽  
Author(s):  
Mingxue Ma ◽  
Yao Ni ◽  
Zirong Chi ◽  
Wanqing Meng ◽  
Haiyang Yu ◽  
...  
Keyword(s):  
Neural Network ◽  
Central Nervous System ◽  
Nervous System ◽  
Long Term Potentiation ◽  
Short Term ◽  
Term Potentiation ◽  
Binary Neural Network ◽  
Neuromorphic Systems ◽  
Human Brains

AbstractThe ability to emulate multiplexed neurochemical transmission is an important step toward mimicking complex brain activities. Glutamate and dopamine are neurotransmitters that regulate thinking and impulse signals independently or synergistically. However, emulation of such simultaneous neurotransmission is still challenging. Here we report design and fabrication of synaptic transistor that emulates multiplexed neurochemical transmission of glutamate and dopamine. The device can perform glutamate-induced long-term potentiation, dopamine-induced short-term potentiation, or co-release-induced depression under particular stimulus patterns. More importantly, a balanced ternary system that uses our ambipolar synaptic device backtrack input ‘true’, ‘false’ and ‘unknown’ logic signals; this process is more similar to the information processing in human brains than a traditional binary neural network. This work provides new insight for neuromorphic systems to establish new principles to reproduce the complexity of a mammalian central nervous system from simple basic units.

Neurotrophins and Proneurotrophins: Focus on Synaptic Activity and Plasticity in the Brain

2017 ◽  
Vol 23 (6) ◽  
pp. 587-604 ◽  
Author(s):  
Julien Gibon ◽  
Philip A. Barker
Keyword(s):  
Long Term Potentiation ◽  
Synaptic Activity ◽  
Cellular Processes ◽  
Term Potentiation ◽  
Neurotrophin 3 ◽  
New Findings ◽  
The Central Nervous System ◽  
The Brain

Neurotrophins have been intensively studied and have multiple roles in the brain. Neurotrophins are first synthetized as proneurotrophins and then cleaved intracellularly and extracellularly. Increasing evidences demonstrate that proneurotrophins and mature neurotrophins exerts opposing role in the central nervous system. In the present review, we explore the role of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT3), and neurotrophin 4 (NT4) and their respective proform in cellular processes related to learning and memory. We focused on their roles in synaptic activity and plasticity in the brain with an emphasis on long-term potentiation, long-term depression, and basal synaptic transmission in the hippocampus and the temporal lobe area. We also discuss new findings on the role of the Val66Met polymorphism on the BDNF propeptide on synaptic activity.

scholarly journals Differential modulation of short-term synaptic dynamics by long-term potentiation at mouse hippocampal mossy fibre synapses

2007 ◽  
Vol 585 (3) ◽  
pp. 853-865 ◽  
Author(s):  
Anja Gundlfinger ◽  
Christian Leibold ◽  
Katja Gebert ◽  
Marion Moisel ◽  
Dietmar Schmitz ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Mossy Fibre ◽  
Differential Modulation ◽  
Short Term ◽  
Term Potentiation ◽  
Synaptic Dynamics

Phosphorylation Changes of CaMKII, ERK1/2, PKB/Akt Kinases and CREB Activation During Early Long-Term Potentiation at Schaffer Collateral-CA1 Mouse Hippocampal Synapses

2009 ◽  
Vol 35 (2) ◽  
pp. 239-246 ◽  
Author(s):  
Mauro Racaniello ◽  
Alessio Cardinale ◽  
Cristiana Mollinari ◽  
Margherita D’Antuono ◽  
Giovanna De Chiara ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Schaffer Collateral ◽  
Creb Activation ◽  
Term Potentiation ◽  
Hippocampal Synapses

Priming-Induced Shift in Synaptic Plasticity in the Rat Hippocampus

1999 ◽  
Vol 82 (4) ◽  
pp. 2024-2028 ◽  
Author(s):  
Hongyan Wang ◽  
John J. Wagner
Keyword(s):  
Synaptic Plasticity ◽  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Crossover Point ◽  
Term Potentiation ◽  
Before And After ◽  
History Of ◽  
The Brain ◽  
Dependent Mechanism

The activity history of a given neuron has been suggested to influence its future responses to synaptic input in one prominent model of experience-dependent synaptic plasticity proposed by Bienenstock, Cooper, and Munro (BCM theory). Because plasticity of synaptic plasticity (i.e., metaplasticity) is similar in concept to aspects of the BCM proposal, we have tested the possibility that a form of metaplasticity induced by a priming stimulation protocol might exhibit BCM-like characteristics. CA1 field excitatory postsynaptic potentials (EPSPs) obtained from rat hippocampal slices were used to monitor synaptic responses before and after conditioning stimuli (3–100 Hz) of the Schaffer collateral inputs. A substantial rightward shift (>5-fold) in the frequency threshold between long-term depression (LTD) and long-term potentiation (LTP) was observed <1 h after priming. This change in the LTD/P crossover point occurred at both primed and unprimed synaptic pathways. These results provide new support for the existence of a rapid, heterosynaptic, experience-dependent mechanism that is capable of modifying the synaptic plasticity phenomena that are commonly proposed to be important for developmental and learning/memory processes in the brain.

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