Role of the glycine site of theN-methyl-d-aspartate receptor in synaptic plasticity induced by pairing

2005 ◽  
Vol 21 (10) ◽  
pp. 2782-2792 ◽  
Author(s):  
N. V. Krasteniakov ◽  
M. Martina ◽  
R. Bergeron
Keyword(s):  
Synaptic Plasticity ◽  
Glycine Site ◽  
Aspartate Receptor

Intraperiaqueductal Gray Glycine and d-Serine Exert Dual Effects on Rostral Ventromedial Medulla on- and off-Cell Activity and Thermoceptive Threshold in the Rat

2009 ◽  
Vol 102 (6) ◽  
pp. 3169-3179 ◽  
Author(s):  
Enza Palazzo ◽  
Francesca Guida ◽  
Annalucia Migliozzi ◽  
Luisa Gatta ◽  
Ida Marabese ◽  
...  
Keyword(s):  
Glycine Receptor ◽  
Cell Activity ◽  
Rostral Ventromedial Medulla ◽  
Tail Flick ◽  
Glycine Site ◽  
Aspartate Receptor ◽  
Tail Flick Latency ◽  
Ventromedial Medulla ◽  
Cell Firing

We have studied the involvement of the N-methyl-d-aspartate receptor (NMDAR) glycine site and the strychnine-sensitive glycine receptor (GlyR) in the ventrolateral periaqueductal gray (VL-PAG) on nociceptive behavior (tail flick) and pain-related changes on neuronal activity in the rostral ventromedial medulla (RVM). Glycine or d-serine increased the tail-flick latency, reduced off-cell pause, and delayed its onset and increased the time between the onset of the off-cell pause and the tail withdrawal. Conversely, they decreased the ongoing activity of the on cell, the tail-flick–induced on-cell firing, whereas they delayed the onset of increased tail-flick–induced on-cell firing. Also, glycine or d-serine reduced the interval between the onset of the increased on-cell firing and tail withdrawal. Whereas 7-Cl-kynurenic acid (7-Cl-KYN) prevented such effects, strychnine did not do so. A higher dose of 7-Cl-KYN or strychnine was per se able to reduce or increase tail-flick latency and increase or reduce on-cell activities, respectively. A higher dose of glycine was hyperalgesic in the presence of 7-Cl-KYN, whereas such an effect was prevented by strychnine. These data suggest 1) a dual role of glycine in producing hyperalgesia or analgesia by stimulating the GlyR or the NMDARs within the VL-PAG, respectively; 2) consistently that RVM on and off cells display opposite firing patterns to the stimulation of the VL-PAG NMDAR glycine site and GlyR activation; and 3) a tonic role of these receptors within the VL-PAG–RVM antinociceptive descending pathway.

Hippocampal ripples down-regulate synapses

Science ◽  
2018 ◽  
Vol 359 (6383) ◽  
pp. 1524-1527 ◽  
Author(s):  
Hiroaki Norimoto ◽  
Kenichi Makino ◽  
Mengxuan Gao ◽  
Yu Shikano ◽  
Kazuki Okamoto ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Neuronal Activity ◽  
Slow Wave ◽  
Down Regulation ◽  
Sharp Wave ◽  
Specific Effects ◽  
Aspartate Receptor ◽  
Specific Input ◽  
Wave States

The specific effects of sleep on synaptic plasticity remain unclear. We report that mouse hippocampal sharp-wave ripple oscillations serve as intrinsic events that trigger long-lasting synaptic depression. Silencing of sharp-wave ripples during slow-wave states prevented the spontaneous down-regulation of net synaptic weights and impaired the learning of new memories. The synaptic down-regulation was dependent on the N-methyl-d-aspartate receptor and selective for a specific input pathway. Thus, our findings are consistent with the role of slow-wave states in refining memory engrams by reducing recent memory-irrelevant neuronal activity and suggest a previously unrecognized function for sharp-wave ripples.

Role of Nicotinic and Muscarinic Receptors on Synaptic Plasticity and Neurological Diseases

2016 ◽  
Vol 22 (14) ◽  
pp. 2004-2014 ◽  
Author(s):  
Marco Fuenzalida ◽  
Miguel Ángel Pérez ◽  
Hugo R. Arias
Keyword(s):  
Synaptic Plasticity ◽  
Muscarinic Receptors ◽  
Neurological Diseases

scholarly journals Dysregulation of Astrocyte–Neuronal Communication in Alzheimer’s Disease

2021 ◽  
Vol 22 (15) ◽  
pp. 7887
Author(s):  
Carmen Nanclares ◽  
Andres Mateo Baraibar ◽  
Alfonso Araque ◽  
Paulo Kofuji
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Synaptic Plasticity ◽  
Neuronal Excitability ◽  
Active Role ◽  
Ionic Homeostasis ◽  
Neuronal Communication ◽  
Structural Support

Recent studies implicate astrocytes in Alzheimer’s disease (AD); however, their role in pathogenesis is poorly understood. Astrocytes have well-established functions in supportive functions such as extracellular ionic homeostasis, structural support, and neurovascular coupling. However, emerging research on astrocytic function in the healthy brain also indicates their role in regulating synaptic plasticity and neuronal excitability via the release of neuroactive substances named gliotransmitters. Here, we review how this “active” role of astrocytes at synapses could contribute to synaptic and neuronal network dysfunction and cognitive impairment in AD.

scholarly journals Monitoring and Modulating Inflammation-Associated Alterations in Synaptic Plasticity: Role of Brain Stimulation and the Blood–Brain Interface

Biomolecules ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 359
Author(s):  
Maximilian Lenz ◽  
Amelie Eichler ◽  
Andreas Vlachos
Keyword(s):  
Synaptic Plasticity ◽  
Brain Stimulation ◽  
Vascular Function ◽  
Neuropsychiatric Symptoms ◽  
Systemic Infection ◽  
Brain Functions ◽  
Blood Brain ◽  
Brain Interface ◽  
The Central Nervous System

Inflammation of the central nervous system can be triggered by endogenous and exogenous stimuli such as local or systemic infection, trauma, and stroke. In addition to neurodegeneration and cell death, alterations in physiological brain functions are often associated with neuroinflammation. Robust experimental evidence has demonstrated that inflammatory cytokines affect the ability of neurons to express plasticity. It has been well-established that inflammation-associated alterations in synaptic plasticity contribute to the development of neuropsychiatric symptoms. Nevertheless, diagnostic approaches and interventional strategies to restore inflammatory deficits in synaptic plasticity are limited. Here, we review recent findings on inflammation-associated alterations in synaptic plasticity and the potential role of the blood–brain interface, i.e., the blood–brain barrier, in modulating synaptic plasticity. Based on recent findings indicating that brain stimulation promotes plasticity and modulates vascular function, we argue that clinically employed non-invasive brain stimulation techniques, such as transcranial magnetic stimulation, could be used for monitoring and modulating inflammation-induced alterations in synaptic plasticity.

The role of elevated autophagy on the synaptic plasticity impairment caused by CdSe/ZnS quantum dots

Biomaterials ◽  
2013 ◽  
Vol 34 (38) ◽  
pp. 10172-10181 ◽  
Author(s):  
Liang Chen ◽  
Yanyan Miao ◽  
Lin Chen ◽  
Peipei Jin ◽  
Yingying Zha ◽  
...  
Keyword(s):  
Quantum Dots ◽  
Synaptic Plasticity

scholarly journals Loss of Non-Apoptotic Role of Caspase-3 in the PINK1 Mouse Model of Parkinson’s Disease

2019 ◽  
Vol 20 (14) ◽  
pp. 3407 ◽  
Author(s):  
Paola Imbriani ◽  
Annalisa Tassone ◽  
Maria Meringolo ◽  
Giulia Ponterio ◽  
Graziella Madeo ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Synaptic Plasticity ◽  
Mouse Model ◽  
Caspase 3 ◽  
Cysteine Proteases ◽  
Synaptic Function ◽  
Adult Brain ◽  
Striatal Slices

Caspases are a family of conserved cysteine proteases that play key roles in multiple cellular processes, including programmed cell death and inflammation. Recent evidence shows that caspases are also involved in crucial non-apoptotic functions, such as dendrite development, axon pruning, and synaptic plasticity mechanisms underlying learning and memory processes. The activated form of caspase-3, which is known to trigger widespread damage and degeneration, can also modulate synaptic function in the adult brain. Thus, in the present study, we tested the hypothesis that caspase-3 modulates synaptic plasticity at corticostriatal synapses in the phosphatase and tensin homolog (PTEN) induced kinase 1 (PINK1) mouse model of Parkinson’s disease (PD). Loss of PINK1 has been previously associated with an impairment of corticostriatal long-term depression (LTD), rescued by amphetamine-induced dopamine release. Here, we show that caspase-3 activity, measured after LTD induction, is significantly decreased in the PINK1 knockout model compared with wild-type mice. Accordingly, pretreatment of striatal slices with the caspase-3 activator α-(Trichloromethyl)-4-pyridineethanol (PETCM) rescues a physiological LTD in PINK1 knockout mice. Furthermore, the inhibition of caspase-3 prevents the amphetamine-induced rescue of LTD in the same model. Our data support a hormesis-based double role of caspase-3; when massively activated, it induces apoptosis, while at lower level of activation, it modulates physiological phenomena, like the expression of corticostriatal LTD. Exploring the non-apoptotic activation of caspase-3 may contribute to clarify the mechanisms involved in synaptic failure in PD, as well as in view of new potential pharmacological targets.

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