Short- and long-term potentiation in afferent pathways of the neonatal rabbit hippocampus

1983 ◽  
Vol 15 (2) ◽  
pp. 124-131
Author(s):  
N. A. Kryuchkova
Keyword(s):  
Long Term Potentiation ◽  
Afferent Pathways ◽  
Rabbit Hippocampus ◽  
Term Potentiation ◽  
Short And Long Term

scholarly journals Long-Term Potentiation and Memory

2004 ◽  
Vol 84 (1) ◽  
pp. 87-136 ◽  
Author(s):  
M. A. LYNCH
Keyword(s):  
Animal Models ◽  
Cell Signaling ◽  
Spatial Learning ◽  
Gene Knockout ◽  
Transgenic Animals ◽  
Long Term Potentiation ◽  
Afferent Pathways ◽  
Term Potentiation ◽  
Signaling Events

Lynch, MA. Long-Term Potentiation and Memory. Physiol Rev 84: 87–136, 2004; 10.1152/physrev.00014.2003.—One of the most significant challenges in neuroscience is to identify the cellular and molecular processes that underlie learning and memory formation. The past decade has seen remarkable progress in understanding changes that accompany certain forms of acquisition and recall, particularly those forms which require activation of afferent pathways in the hippocampus. This progress can be attributed to a number of factors including well-characterized animal models, well-defined probes for analysis of cell signaling events and changes in gene transcription, and technology which has allowed gene knockout and overexpression in cells and animals. Of the several animal models used in identifying the changes which accompany plasticity in synaptic connections, long-term potentiation (LTP) has received most attention, and although it is not yet clear whether the changes that underlie maintenance of LTP also underlie memory consolidation, significant advances have been made in understanding cell signaling events that contribute to this form of synaptic plasticity. In this review, emphasis is focused on analysis of changes that occur after learning, especially spatial learning, and LTP and the value of assessing these changes in parallel is discussed. The effect of different stressors on spatial learning/memory and LTP is emphasized, and the review concludes with a brief analysis of the contribution of studies, in which transgenic animals were used, to the literature on memory/learning and LTP.

scholarly journals Endocannabinoid dynamics gate spike-timing dependent depression and potentiation

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Yihui Cui ◽  
Ilya Prokin ◽  
Hao Xu ◽  
Bruno Delord ◽  
Stephane Genet ◽  
...  
Keyword(s):  
Mathematical Modeling ◽  
Synaptic Plasticity ◽  
Learning And Memory ◽  
Long Term Potentiation ◽  
Cellular Mechanism ◽  
Spike Timing ◽  
Long Term Depression ◽  
Term Potentiation ◽  
Short And Long Term

Synaptic plasticity is a cardinal cellular mechanism for learning and memory. The endocannabinoid (eCB) system has emerged as a pivotal pathway for synaptic plasticity because of its widely characterized ability to depress synaptic transmission on short- and long-term scales. Recent reports indicate that eCBs also mediate potentiation of the synapse. However, it is not known how eCB signaling may support bidirectionality. Here, we combined electrophysiology experiments with mathematical modeling to question the mechanisms of eCB bidirectionality in spike-timing dependent plasticity (STDP) at corticostriatal synapses. We demonstrate that STDP outcome is controlled by eCB levels and dynamics: prolonged and moderate levels of eCB lead to eCB-mediated long-term depression (eCB-tLTD) while short and large eCB transients produce eCB-mediated long-term potentiation (eCB-tLTP). Moreover, we show that eCB-tLTD requires active calcineurin whereas eCB-tLTP necessitates the activity of presynaptic PKA. Therefore, just like glutamate or GABA, eCB form a bidirectional system to encode learning and memory.

scholarly journals Design and Characterization of Semi-Floating-Gate Synaptic Transistor

Micromachines ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 32 ◽  
Author(s):  
Yongbeom Cho ◽  
Jae Yoon Lee ◽  
Eunseon Yu ◽  
Jae-Hee Han ◽  
Myung-Hyun Baek ◽  
...  
Keyword(s):  
Long Term Potentiation ◽  
Spike Timing ◽  
Floating Gate ◽  
Total System ◽  
Charge Trap ◽  
Tunneling Mechanism ◽  
Integration Density ◽  
Term Potentiation ◽  
Short And Long Term

In this work, a study on a semi-floating-gate synaptic transistor (SFGST) is performed to verify its feasibility in the more energy-efficient hardware-driven neuromorphic system. To realize short- and long-term potentiation (STP/LTP) in the SFGST, a poly-Si semi-floating gate (SFG) and a SiN charge-trap layer are utilized, respectively. When an adequate number of holes are accumulated in the SFG, they are injected into the nitride charge-trap layer by the Fowler–Nordheim tunneling mechanism. Moreover, since the SFG is charged by an embedded tunneling field-effect transistor existing between the channel and the drain junction when the post-synaptic spike occurs after the pre-synaptic spike, and vice versa, the SFG is discharged by the diode when the post-synaptic spike takes place before the pre-synaptic spike. This indicates that the SFGST can attain STP/LTP and spike-timing-dependent plasticity behaviors. These characteristics of the SFGST in the highly miniaturized transistor structure can contribute to the neuromorphic chip such that the total system may operate as fast as the human brain with low power consumption and high integration density.

scholarly journals GluA2-dependent AMPA receptor endocytosis and the decay of early and late long-term potentiation: possible mechanisms for forgetting of short- and long-term memories

2014 ◽  
Vol 369 (1633) ◽  
pp. 20130141 ◽  
Author(s):  
Oliver Hardt ◽  
Karim Nader ◽  
Yu-Tian Wang
Keyword(s):  
Ampa Receptors ◽  
Long Term Potentiation ◽  
Homeostatic Plasticity ◽  
Molecular Processes ◽  
Short Term ◽  
Receptor Endocytosis ◽  
Term Potentiation ◽  
Short And Long Term ◽  
Activity Dependent

The molecular processes involved in establishing long-term potentiation (LTP) have been characterized well, but the decay of early and late LTP (E-LTP and L-LTP) is poorly understood. We review recent advances in describing the mechanisms involved in maintaining LTP and homeostatic plasticity. We discuss how these phenomena could relate to processes that might underpin the loss of synaptic potentiation over time, and how they might contribute to the forgetting of short-term and long-term memories. We propose that homeostatic downscaling mediates the loss of E-LTP, and that metaplastic parameters determine the decay rate of L-LTP, while both processes require the activity-dependent removal of postsynaptic GluA2-containing AMPA receptors.

Differing Mechanisms of Expression for Short- and Long-Term Potentiation

1997 ◽  
Vol 78 (1) ◽  
pp. 321-334 ◽  
Author(s):  
Paul E. Schulz ◽  
Jill C. Fitzgibbons
Keyword(s):  
Synaptic Plasticity ◽  
Extracellular Recording ◽  
Long Term Potentiation ◽  
Memory Storage ◽  
High Frequency Stimulation ◽  
Excitatory Postsynaptic Potential ◽  
Induction Step ◽  
Term Potentiation ◽  
Short And Long Term

Schulz, Paul E. and Jill C. Fitzgibbons. Differing mechanisms of expression for short- and long-term potentiation. J. Neurophysiol. 78: 321–334, 1997. Long-term potentiation (LTP) is a use-dependent form of synaptic plasticity that is of great interest as a cellular mechanism that may contribute to memory storage. It is the sustained phase of population excitatory postsynaptic potential induced by high-frequency stimulation (HFS). HFS can also induce short-term potentiation (STP), a decremental potentiation lasting ∼15 min. It has been unclear whether STP is simply a reversible form of LTP elicited by subthreshold stimuli or whether it is an independently expressed form of synaptic plasticity. We have attempted to clarify the relationship between LTP and STP in the extracellular recording technique in area CA1 of the adult rat hippocampal slice preparation to test four predictions of the hypothesis that LTP and STP are expressed via the same mechanism. First, occluding LTP expression should block STP expression. Saturating LTP under six different conditions, however, did not occlude STP expression. Second, occluding STP expression should occlude LTP expression. The partial or full occlusion of STP by two maneuvers (increasing the stimulus intensity used for HFS or applying 3-isobutyl-1-methylxanthine), however, did not occlude LTP expression. Third, LTP increases and decreases paired-pulse facilitation (PPF), and STP should have the same effect. STP did not change PPF, however. The first three results, then, suggest that STP and LTP are expressed via different mechanisms. Fourth, STP should be maximal near the LTP induction threshold, and then decrease above it. Surprisingly, STP was maximal at or very close to the LTP induction threshold, but it did not decrease above this threshold. This relationship suggests the possibility that STP and LTP share an induction step(s). What is the function of the independently expressed STP? We find that LTP can be induced by two HFSs, each of which is subthreshold for LTP, if the second is given during STP from the first. This suggests that STP can temporarily lower the LTP induction threshold. Three lines of evidence, then, suggest that STP and LTP may be expressed via different mechanisms; however, the proximity of STP saturation to LTP induction suggests that they may share an induction step(s). STP may also have the very important function of temporarily lowering the LTP induction threshold. Finally, these data suggestion caution in interpreting LTP data obtained <20–30 min after HFS, because they may be contaminated by STP, which appears to have different underlying mechanisms.

scholarly journals Neurotransmission and neuromodulation systems in the learning and memory network of Octopus vulgaris

2021 ◽  
Author(s):  
Naama Stern-mentch ◽  
Gabrielle Winters Carrington ◽  
Michael Belenky ◽  
Leonid L. Moroz ◽  
Binyamin Hochner
Keyword(s):  
Learning And Memory ◽  
Long Term Potentiation ◽  
Octopus Vulgaris ◽  
Connectivity Matrix ◽  
Term Potentiation ◽  
Memory Network ◽  
Short And Long Term ◽  
Deep Nucleus ◽  
Efficient Learning

The vertical lobe (VL) in the octopus brain plays an essential role in its sophisticated learning and memory. Early anatomical studies suggested that the VL is organized in a fan-out fan-in connectivity matrix comprising only three morphologically identified neuron types; input axons from the superior frontal lobe (SFL) innervating en passant millions of small amacrine interneurons (AMs) which converge sharply onto large VL output neurons (LNs). Recent physiological studies confirmed the feedforward excitatory connectivity: a glutamatergic synapse at the first SFL-to-AM synaptic layer and a cholinergic AM-to-LNs synapse. SFL-to-AMs synapses show a robust hippocampal-like activity-dependent long-term potentiation (LTP) of transmitter release. 5-HT, octopamine, dopamine and nitric oxide modulate short- and long-term VL synaptic plasticity. Here we present a comprehensive histolabeling study to better characterize the neural elements in the VL. We generally confirmed glutamatergic SFLs and cholinergic AMs. Intense labeling for NOS activity in the AMs neurites fitted with the NO-dependent presynaptic LTP mechanism at the SFL-to-AM synapse. New discoveries here reveal more heterogeneity of the VL neurons than previously thought. GABAergic AMs suggest a subpopulation of inhibitory interneurons in the first input layer. Clear GABA labeling in the cell bodies of LNs supported an inhibitory VL output yet the LNs co-expressed FMRFamide-like neuropeptides suggesting an additional neuromodulatory role of the VL output. Furthermore, a group of LNs was glutamatergic. A new cluster of cells organized in a deep nucleus showed rich catecholaminergic labeling and may play a role in intrinsic neuromodulation. In situ hybridization and immunolabeling allowed characterization and localization of a rich array of neuropeptides and neuromodulatores, likely involved in reward/punishment signals. This analysis of the fast transmission system, together with the newly found cellular elements helps integrate behavioral, physiological, pharmacological and connectome findings into a more comprehensive understanding of an efficient learning and memory network

A Kinetic Model of Short- and Long-Term Potentiation

1993 ◽  
Vol 5 (4) ◽  
pp. 636-647 ◽  
Author(s):  
M. Migliore ◽  
G. F. Ayala
Keyword(s):  
Kinetic Model ◽  
Long Term Potentiation ◽  
High Frequency Stimulation ◽  
Term Change ◽  
Term Potentiation ◽  
Frequency Stimulation ◽  
Short And Long Term ◽  
Experimental Findings ◽  
Retrograde Signal

We present a kinetic model that can account for several experimental findings on short- and long-term potentiation (STP and LTP) and their pharmacological modulation. The model, which is consistent with Hebb's postulate, uses the hypothesis that part of the origin of LTP may be a consequence of an increased release of neurotransmitter due to a retrograde signal. The operation of the model is expressed by a set of irreversible reactions, each of which should be thought of as equivalent to a set of more complex reactions. We show that a retrograde signal alone is not sufficient to maintain LTP unless long-term change of the rate constant of some of the reactions is caused by high-frequency stimulation. Pharmacological manipulation of LTP is interpreted as modifications of the rate constants of one or more of the reactions that express a given mechanism. The model, because of its simplicity, can be useful to test more specific mechanisms by expanding one or more reactions as suggested by new experimental evidence.

Exogenous glutamate induces short and long-term potentiation in the rat medial vestibular nuclei

Neuroreport ◽  
2001 ◽  
Vol 12 (11) ◽  
pp. 2329-2334 ◽  
Author(s):  
Silvarosa Grassi ◽  
Adele Frondaroli ◽  
Mauro Pessia ◽  
Vito Enrico Pettorossi
Keyword(s):  
Vestibular Nuclei ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Short And Long Term
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