Facial nerve axotomy induces changes on hippocampal CA3-to-CA1 long-term synaptic plasticity

In spike-timing-dependent plasticity (STDP), the direction and degree of synaptic modification are determined by the coherence of pre- and postsynaptic activities within a neuron. However, in the adult rat hippocampus, it remains unclear whether STDP-like mechanisms in a neuronal population induce synaptic potentiation of a long duration. Thus, we asked whether the magnitude and maintenance of synaptic plasticity in a population of CA1 neurons differ as a function of the temporal order and interval between pre- and postsynaptic activities. Modulation of the relative timing of Schaffer collateral fibers (presynaptic component) and CA1 axons (postsynaptic component) stimulations resulted in an asymmetric population STDP (pSTDP). The resulting potentiation in response to 20 pairings at 1 Hz was largest in magnitude and most persistent (4 h) when presynaptic activity coincided with or preceded postsynaptic activity. Interestingly, when postsynaptic activation preceded presynaptic stimulation by 20 ms, an immediate increase in field excitatory postsynaptic potentials was observed, but it eventually transformed into a synaptic depression. Furthermore, pSTDP engaged in selective forms of late-associative activity: It facilitated the maintenance of tetanization-induced early long-term potentiation (LTP) in neighboring synapses but not early long-term depression, reflecting possible mechanistic differences with classical tetanization-induced LTP. The data demonstrate that a pairing of pre- and postsynaptic activities in a neuronal population can greatly reduce the required number of synaptic plasticity-evoking events and induce a potentiation of a degree and duration similar to that with repeated tetanization. Thus, pSTDP determines synaptic efficacy in the hippocampal CA3–CA1 circuit and could bias the CA1 neuronal population toward potentiation in future events.

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CAPS1 is involved in hippocampal synaptic plasticity and hippocampus-associated learning

Scientific Reports ◽

10.1038/s41598-021-88009-w ◽

2021 ◽

Vol 11 (1) ◽

Author(s):

Chiaki Ishii ◽

Natsumi Shibano ◽

Mio Yamazaki ◽

Tomoki Arima ◽

Yuna Kato ◽

...

Keyword(s):

Synaptic Plasticity ◽

Long Term Potentiation ◽

Conditional Knockout ◽

Cellular Mechanisms ◽

Adeno Associated Virus ◽

Calcium Dependent ◽

Term Potentiation ◽

Hippocampal Ca3 ◽

Vesicular Exocytosis

AbstractCalcium-dependent activator protein for secretion 1 (CAPS1) is a key molecule in vesicular exocytosis, probably in the priming step. However, CAPS1’s role in synaptic plasticity and brain function is elusive. Herein, we showed that synaptic plasticity and learning behavior were impaired in forebrain and/or hippocampus-specific Caps1 conditional knockout (cKO) mice by means of molecular, physiological, and behavioral analyses. Neonatal Caps1 cKO mice showed a decrease in the number of docked vesicles in the hippocampal CA3 region, with no detectable changes in the distribution of other major exocytosis-related molecules. Additionally, long-term potentiation (LTP) was partially and severely impaired in the CA1 and CA3 regions, respectively. CA1 LTP was reinforced by repeated high-frequency stimuli, whereas CA3 LTP was completely abolished. Accordingly, hippocampus-associated learning was severely impaired in adeno-associated virus (AAV) infection-mediated postnatal Caps1 cKO mice. Collectively, our findings suggest that CAPS1 is a key protein involved in the cellular mechanisms underlying hippocampal synaptic release and plasticity, which is crucial for hippocampus-associated learning.

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SCRAPPER Regulates the Thresholds of Long-Term Potentiation/Depression, the Bidirectional Synaptic Plasticity in Hippocampal CA3-CA1 Synapses

Neural Plasticity ◽

10.1155/2012/352829 ◽

2012 ◽

Vol 2012 ◽

pp. 1-7 ◽

Cited By ~ 6

Author(s):

Hiroshi Takagi ◽

Mitsutoshi Setou ◽

Seiji Ito ◽

Ikuko Yao

Keyword(s):

Synaptic Plasticity ◽

Hippocampal Slices ◽

Low Frequency ◽

Long Term Potentiation ◽

Low Frequency Stimulation ◽

Term Potentiation ◽

Hippocampal Ca3 ◽

Frequency Stimulation ◽

F Box Protein

SCRAPPER, which is an F-box protein encoded byFBXL20, regulates the frequency of the miniature excitatory synaptic current through the ubiquitination of Rab3-interacting molecule 1. Here, we recorded the induction of long-term potentiation/depression (LTP/LTD) in CA3-CA1 synapses in E3 ubiquitin ligase SCRAPPER-deficient hippocampal slices. Compared to wild-type mice,Scrapper-knockout mice exhibited LTDs with smaller magnitudes after induction with low-frequency stimulation and LTPs with larger magnitudes after induction with tetanus stimulation. These findings suggest that SCRAPPER regulates the threshold of bidirectional synaptic plasticity and, therefore, metaplasticity.

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Immune Challenge Alters Reactivity of Hippocampal Noradrenergic System in Prenatally Stressed Aged Mice

Neural Plasticity ◽

10.1155/2019/3152129 ◽

2019 ◽

Vol 2019 ◽

pp. 1-13 ◽

Cited By ~ 1

Author(s):

Gayane Grigoryan ◽

Niklas Lonnemann ◽

Martin Korte

Keyword(s):

Synaptic Plasticity ◽

Structural Integrity ◽

Corticosterone Level ◽

Long Term Potentiation ◽

Aging Brain ◽

Aged Mice ◽

Hippocampal Synaptic Plasticity ◽

Term Potentiation ◽

Hippocampal Ca3

Prenatal stress (PS) has long-term sequelae for the morphological and functional status of the central nervous system of the progeny. A PS-induced proinflammatory status of the organism may result in an impairment of both hippocampal synaptic plasticity and hippocampus-dependent memory formation in adults. We addressed here the question of how PS-induced alterations in the immune response in young and old mice may contribute to changes in hippocampal function in aging. Immune stimulation (via LPS injection) significantly affected the ability of the hippocampal CA3-CA1 synapse of PS mice to undergo long-term potentiation (LTP). Elevated corticosterone level in the blood of aged PS mice that is known to influence LTP magnitude indicates a chronic activation of the HPA axis due to the in utero stress exposure. We investigated the contribution of adrenergic receptors to the modulation of hippocampal synaptic plasticity of aged mice and found that impaired LTP in the PS-LPS group was indeed rescued by application of isoproterenol (a nonspecific noradrenergic agonist). Further exploration of the mechanisms of the observed phenomena will add to our understanding of the interaction between PS and proinflammatory immune activation and its contribution to the functional and structural integrity of the aging brain.

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Modulation of Ca2+ currents and long-term synaptic plasticity by SSRIs

Pharmacopsychiatry ◽

10.1055/s-2003-825454 ◽

2004 ◽

Vol 36 (05) ◽

Author(s):

C Normann

Keyword(s):

Synaptic Plasticity

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Translational Control of Long-Term Synaptic Plasticity and Memory Storage by eIF2α

Critical Reviews in Neurobiology ◽

10.1615/critrevneurobiol.v18.i1-2.190 ◽

2006 ◽

Vol 18 (1-2) ◽

pp. 187-195 ◽

Cited By ~ 12

Author(s):

Nahum Sonenberg ◽

Mauro Costa-Mattioli

Keyword(s):

Synaptic Plasticity ◽

Translational Control ◽

Memory Storage

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The Effects of P75NTR on Learning Memory Mediated by Hippocampal Apoptosis and Synaptic Plasticity

Current Pharmaceutical Design ◽

10.2174/1381612826666200916145142 ◽

2020 ◽

Vol 26 ◽

Author(s):

Jun-Jie Tang ◽

Shuang Feng ◽

Xing-Dong Chen ◽

Hua Huang ◽

Min Mao ◽

...

Keyword(s):

Synaptic Plasticity ◽

Learning And Memory ◽

Neurological Diseases ◽

Neurotrophin Receptor ◽

P75 Neurotrophin Receptor ◽

Negative Effects ◽

Apoptotic Effect ◽

New Ideas ◽

The Relationship

: Neurological diseases bring great mental and physical torture to the patients, and have long-term and sustained negative effects on families and society. The attention to neurological diseases is increasing, and the improvement of the material level is accompanied by an increase in the demand for mental level. The p75 neurotrophin receptor (p75NTR) is a low-affinity neurotrophin receptor and involved in diverse and pleiotropic effects in the developmental and adult central nervous system (CNS). Since neurological diseases are usually accompanied by the regression of memory, the pathogenesis of p75NTR also activates and inhibits other signaling pathways, which has a serious impact on the learning and memory of patients. The results of studies shown that p75NTR is associated with LTP/LTD-induced synaptic enhancement and inhibition, suggest that p75NTR may be involved in the progression of synaptic plasticity. And its pro-apoptotic effect is associated with activation of proBDNF and inhibition of proNGF, and TrkA/p75NTR imbalance leads to pro-survival or pro-apoptotic phenomena. It can be inferred that p75NTR mediates apoptosis in the hippocampus and amygdale, which may affect learning and memory behavior. This article mainly discusses the relationship between p75NTR and learning memory and associated mechanisms, which may provide some new ideas for the treatment of neurological diseases.

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Brivaracetam Prevents the Over-expression of Synaptic Vesicle Protein 2A and Rescues the Deficits of Hippocampal Long-term Potentiation In Vivo in Chronic Temporal Lobe Epilepsy Rats

Current Neurovascular Research ◽

10.2174/1567202617666200514114917 ◽

2020 ◽

Vol 17 (4) ◽

pp. 354-360 ◽

Cited By ~ 1

Author(s):

Yu-Xing Ge ◽

Ying-Ying Lin ◽

Qian-Qian Bi ◽

Yu-Juan Chen

Keyword(s):

Synaptic Plasticity ◽

Temporal Lobe Epilepsy ◽

Synaptic Vesicle ◽

Long Term Potentiation ◽

Synaptic Dysfunction ◽

Over Expression ◽

Term Potentiation ◽

Synaptic Vesicle Protein 2A

Background: Patients with temporal lobe epilepsy (TLE) usually suffer from cognitive deficits and recurrent seizures. Brivaracetam (BRV) is a novel anti-epileptic drug (AEDs) recently used for the treatment of partial seizures with or without secondary generalization. Different from other AEDs, BRV has some favorable properties on synaptic plasticity. However, the underlying mechanisms remain elusive. Objective: The aim of this study was to explore the neuroprotective mechanism of BRV on synaptic plasticity in experimental TLE rats. Methods: The effect of chronic treatment with BRV (10 mg/kg) was assessed on Pilocarpine induced TLE model through measurement of the field excitatory postsynaptic potentials (fEPSPs) in vivo. Differentially expressed synaptic vesicle protein 2A (SV2A) were identified with immunoblot. Then, fast phosphorylation of synaptosomal-associated protein 25 (SNAP-25) during long-term potentiation (LTP) induction was performed to investigate the potential roles of BRV on synaptic plasticity in the TLE model. Results: An increased level of SV2A accompanied by a depressed LTP in the hippocampus was shown in epileptic rats. Furthermore, BRV treatment continued for more than 30 days improved the over-expression of SV2A and reversed the synaptic dysfunction in epileptic rats. Additionally, BRV treatment alleviates the abnormal SNAP-25 phosphorylation at Ser187 during LTP induction in epileptic ones, which is relevant to the modulation of synaptic vesicles exocytosis and voltagegated calcium channels. Conclusion: BRV treatment ameliorated the over-expression of SV2A in the hippocampus and rescued the synaptic dysfunction in epileptic rats. These results identify the neuroprotective effect of BRV on TLE model.

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Long-term results of microvascular free-tissue transfer reanimation of the paralyzed face: Three cases

Ear Nose & Throat Journal ◽

10.1177/014556130808700416 ◽

2008 ◽

Vol 87 (4) ◽

pp. 226-233

Author(s):

John P. Leonetti ◽

Chad A. Zender ◽

Daryl Vandevender ◽

Sam J. Marzo

Keyword(s):

Facial Nerve ◽

Academic Medical Center ◽

Tertiary Care ◽

Free Tissue Transfer ◽

Long Term Results ◽

Wide Field ◽

Facial Movement ◽

Tissue Transfer ◽

Facial Reanimation

We conducted a retrospective case review at our tertiary care academic medical center to assess the long-term results of microvascular free-tissue transfer to achieve facial reanimation in 3 patients. These patients had undergone wide-field parotidectomy with facial nerve resection. Upper facial reanimation was accomplished with a proximal facial nerve–sural nerve graft, and lower facial movement was achieved through proximal facial nerve–long thoracic (serratus muscle) nerve anastomosis. Outcomes were determined by grading postoperative facial nerve function according to the House-Brackmann system. All 3 patients were able to close their eyes independent of lower facial movement, and all 3 had achieved House-Brackmann grade III function. We conclude that reanimating the paralyzed face with microvascular free-tissue transfer provides anatomic coverage and mimetic function after wide-field parotidectomy. Synkinesis is reduced by separating upper-and lower-division reanimation.

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