Presenilins are essential for regulating neurotransmitter release
Chen ZhangBei WuVassilios BeglopoulosMary Wines-SamuelsonDawei ZhangIoannis DragatsisThomas C. SüdhofJie Shen
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Neural facilitation
Thapsigargin
Sodium nitroprusside
Long-term depression
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WE have investigated the interaction between long-term potentiation (LTP) and paired-pulse facilitation (PPF) in the hippocampal CA1 region under different conditions of initial PPF. PPF is a short lasting presynaptic alteration in synaptic efficacy, determined by the presynaptic release probability, where a high and low PPF indicate a low and high release probability, respectively. LTP was associated with no, or only little, change in PPF, independent of the initial value of PPF and of the time of measurement within the first hour of LTP. These results support the notion that the expression mechanism of LTP is not regulated by the initial release probability and that LTP is due to a single expression mechanism within its first hour.
Facilitation
Neural facilitation
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Nonsynaptic plasticity
Synaptic scaling
Homosynaptic plasticity
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The paper reviews the effect of a traditional Chinese medical prescription,Kaixinsan on synaptic plasticity, long-term potentiation,and demonstrates that Kaixinsan can promote the formation of long-term potentiation of synaptic transmission and antagonize the inhibitory effect of some substances for long-term potentiation,suggesting an effective function of the promotion of memory and learning.
Homosynaptic plasticity
Synaptic scaling
Nonsynaptic plasticity
Promotion (chess)
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Evidence indicates that inhalative anesthetics enhance the β-site amyloid precursor protein (APP)-cleaving enzyme (BACE) activity, increase amyloid beta 1-42 (Aβ1-42) aggregation, and modulate dendritic spine dynamics. However, the mechanisms of inhalative anesthetics on hippocampal dendritic spine plasticity and BACE-dependent APP processing remain unclear. In this study, hippocampal slices were incubated with equipotent isoflurane (iso), sevoflurane (sevo), or xenon (Xe) with/without pretreatment of the BACE inhibitor LY2886721 (LY). Thereafter, CA1 dendritic spine density, APP processing-related molecule expressions, nectin-3 levels, and long-term potentiation (LTP) were tested. The nectin-3 downregulation on LTP and dendritic spines were evaluated. Sevo treatment increased hippocampal mouse Aβ1-42 (mAβ1-42), abolished CA1-LTP, and decreased spine density and nectin-3 expressions in the CA1 region. Furthermore, CA1-nectin-3 knockdown blocked LTP and reduced spine density. Iso treatment decreased spine density and attenuated LTP. Although Xe blocked LTP, it did not affect spine density, mAβ1-42, or nectin-3. Finally, antagonizing BACE activity partly restored sevo-induced deficits. Taken together, our study suggests that sevo partly elevates BACE activity and interferes with synaptic remodeling, whereas iso mildly modulates synaptic changes in the CA1 region of the hippocampus. On the other hand, Xe does not alternate dendritic spine remodeling.
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Thapsigargin
LTP induction
Calcium in biology
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Neurotrophins have been implicated in activity-dependent synaptic plasticity, but the underlying intracellular mechanisms remain largely unknown. Synaptic potentiation induced by brain-derived neurotrophic factor (BDNF), but not neurotrophin 3, was prevented by blockers of adenosine 3',5'-monophosphate (cAMP) signaling. Activators of cAMP signaling alone were ineffective in modifying synaptic efficacy but greatly enhanced the potentiation effect of BDNF. Blocking cAMP signaling abolished the facilitation of BDNF-induced potentiation by presynaptic activity. Thus synaptic actions of BDNF are gated by cAMP. Activity and other coincident signals that modulate cAMP concentrations may specify the action of secreted neurotrophins on developing nerve terminals.
Nonsynaptic plasticity
Neural facilitation
Cyclic adenosine monophosphate
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The long-lasting increase in synaptic strength known as long-term potentiation has been advanced as a potential physiological mechanism for many forms of both developmental and adult neuronal plasticity. In many models of plasticity, intercellular communication has been proposed to account for observations in which simultaneously active neurons are strengthened together. The data presented here indicate that long-term potentiation can be communicated between synapses on neighboring neurons by means of a diffusible messenger. This distributed potentiation provides a mechanism for the cooperative strengthening of proximal synapses and may underlie a variety of plastic processes in the nervous system.
Synaptic scaling
Nonsynaptic plasticity
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Abstract Since the discovery of long‐term potentiation ( LTP ) about a half‐century ago, Ca 2+ /CaM‐dependent protein kinase II (Ca MKII ) has been one of the most extensively studied components of the molecular machinery that regulate plasticity. This unique dodecameric kinase complex plays pivotal roles in LTP by phosphorylating substrates through elaborate regulatory mechanisms, and is known to be both necessary and sufficient for LTP . In addition to acting as a kinase, Ca MKII has been postulated to have structural roles because of its extraordinary abundance and diverse interacting partners. It now is becoming clear that these two functions of Ca MKII cooperate closely for the induction of both functional and structural synaptic plasticity of dendritic spines. image Because of its extraordinary abundance within neuronal cells, calmodulin kinase Ca MKII has been believed to act as a structural protein as well as an enzyme during synaptic plasticity. In this review, we summarized studies in Ca MKII field and provide an insight into how enzymatic and structural functions of Ca MKII cooperate with each other for long‐term potentiation ( LTP ) in neurons. This article is part of a mini review series: “Synaptic Function and Dysfunction in Brain Diseases” .
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