A common rule governs the synaptic locus of both short-term and long-term potentiation

1993 ◽  
Vol 3 (12) ◽  
pp. 832-841 ◽  
Author(s):  
Timo Hannay ◽  
Alan Larkman ◽  
Ken Stratford ◽  
Julian Jack
Keyword(s):  
Long Term Potentiation ◽  
Short Term ◽  
Common Rule ◽  
Term Potentiation

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.

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

Short-term plasticity and long-term potentiation mimicked in single inorganic synapses

2011 ◽  
Vol 10 (8) ◽  
pp. 591-595 ◽  
Author(s):  
Takeo Ohno ◽  
Tsuyoshi Hasegawa ◽  
Tohru Tsuruoka ◽  
Kazuya Terabe ◽  
James K. Gimzewski ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Short Term ◽  
Short Term Plasticity ◽  
Term Potentiation

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.

Global Action against Dementia Call for Innovations

2016 ◽  
Vol 2 (4) ◽  
pp. 260-274
Author(s):  
Dajue Wang
Keyword(s):  
Entorhinal Cortex ◽  
Hippocampal Formation ◽  
Long Term Potentiation ◽  
Animal Assisted Therapy ◽  
Current Status ◽  
Short Term ◽  
Term Memory ◽  
Term Potentiation ◽  
Pharmaceutical Industries

With the fast-growing aging population, dementia has become a health priority. However, in the past, medicine was largely dealing with physical disorders, and not enough knowledge and experience have been accumulated for mental health. The main and first symptom of this disorder is the loss of memory; hence, understanding the hippocampal formation is the key to tackling dementia. In 2007, a milestone book titled “Hippocampus Book” was published. One of the authors/editors is the 2014 Nobel Laureate in Physiology and Medicine, Professor John O'Keefe. It is a MUST-READ encyclopedia about the hippocampal formation, for those who wish to commit themselves to helping the patients with dementia. The formation consists of the hippocampus, entorhinal cortex, subiculum, presubiculum, parasubiculum, and dentate gyrus. The hippocampus is further divided into CA1, CA2, and CA3. The entorhinal cortex is the gateway of receiving all sensory information from the neocortex, while the subiculum is the exit for the efferent projections to the neocortex. Memory is divided into short-term and long-term memory. The former does not require protein synthesis while the latter does. The electrophysiological activities of creating these memories are short-term potentiation and long-term potentiation respectively. In most cases, the entorhinal cortex is the first structure to be damaged, and even short-term memory cannot be created. However, all except spatial memory are stored in the neocortex. Damage to the hippocampal formation would not affect the storage and retrieval of memories. Hence, past memories may remain intact in the early phases of the disorder. This devastating progressive disease has no cure. However, the highly plastic hippocampal formation may offer us some hope. It is the responsibility of the pharmaceutical industries to develop new drugs. Clinicians should add their efforts to the endeavor. The author would suggest that they explore insulin-like growth factors, brain stimulation, cell transplantation, and animal-assisted therapy to find some innovative solutions to help patients with dementia. As the current status of neuroscience stands, the animal-assisted therapy seems to stand out among all methods. It alleviates symptoms and stabilizes the ailment.

scholarly journals Short-Term High-Fat-and-Fructose Feeding Produces Insulin Signaling Alterations Accompanied by Neurite and Synaptic Reduction and Astroglial Activation in the Rat Hippocampus

2014 ◽  
Vol 34 (6) ◽  
pp. 1001-1008 ◽  
Author(s):  
Erika Calvo-Ochoa ◽  
Karina Hernández-Ortega ◽  
Patricia Ferrera ◽  
Sumiko Morimoto ◽  
Clorinda Arias
Keyword(s):  
Insulin Resistance ◽  
Insulin Signaling ◽  
Control Diet ◽  
Long Term Potentiation ◽  
High Fat ◽  
Short Term ◽  
Term Potentiation ◽  
High Fructose ◽  
High Fructose Syrup

Chronic consumption of high-fat-and-fructose diets (HFFD) is associated with the development of insulin resistance (InsRes) and obesity. Systemic insulin resistance resulting from long-term HFFD feeding has detrimental consequences on cognitive performance, neurogenesis, and long-term potentiation establishment, accompanied by neuronal alterations in the hippocampus. However, diet-induced hippocampal InsRes has not been reported. Therefore, we investigated whether short-term HFFD feeding produced hippocampal insulin signaling alterations associated with neuronal changes in the hippocampus. Rats were fed with a control diet or an HFFD consisting of 10% lard supplemented chow and 20% high-fructose syrup in the drinking water. Our results show that 7 days of HFFD feeding induce obesity and InsRes, associated with the following alterations in the hippocampus: (1) a decreased insulin signaling; (2) a decreased hippocampal weight; (3) a reduction in dendritic arborization in CA1 and microtubule-associated protein 2 (MAP-2) levels; (4) a decreased dendritic spine number in CA1 and synaptophysin content, along with an increase in tau phosphorylation; and finally, (5) an increase in reactive astrocyte associated with microglial changes. To our knowledge, this is the first report addressing hippocampal insulin signaling, as well as morphologic, structural, and functional modifications due to short-term HFFD feeding in the rat.

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