scholarly journals Molecular Mechanisms of Short-Term Plasticity: Role of Synapsin Phosphorylation in Augmentation and Potentiation of Spontaneous Glutamate Release

2018 ◽  
Vol 10 ◽  
Author(s):  
Qing Cheng ◽  
Sang-Ho Song ◽  
George J. Augustine
Keyword(s):  
Molecular Mechanisms ◽  
Glutamate Release ◽  
Short Term ◽  
Short Term Plasticity

scholarly journals The Role of NMDA Receptor Subtypes in Short-Term Plasticity in the Rat Entorhinal Cortex

2008 ◽  
Vol 2008 ◽  
pp. 1-13 ◽  
Author(s):  
Sophie E. L. Chamberlain ◽  
Jian Yang ◽  
Roland S. G. Jones
Keyword(s):  
Entorhinal Cortex ◽  
Glutamate Release ◽  
Receptor Subtypes ◽  
Short Term ◽  
Low Frequencies ◽  
Short Term Plasticity ◽  
Whole Cell Patch Clamp ◽  
Layer V ◽  
Presynaptic Nmda Receptors

We have previously shown that spontaneous release of glutamate in the entorhinal cortex (EC) is tonically facilitated via activation of presynaptic NMDA receptors (NMDAr) containing the NR2B subunit. Here we show that the same receptors mediate short-term plasticity manifested by frequency-dependent facilitation of evoked glutamate release at these synapses. Whole-cell patch-clamp recordings were made from layer V pyramidal neurones in rat EC slices. Evoked excitatory postsynaptic currents showed strong facilitation at relatively low frequencies (3 Hz) of activation. Facilitation was abolished by an NR2B-selective blocker (Ro 25-6981), but unaffected by NR2A-selective antagonists (Zn2+, NVP-AAM077). In contrast, postsynaptic NMDAr-mediated responses could be reduced by subunit-selective concentrations of all three antagonists. The data suggest that NMDAr involved in presynaptic plasticity in layer V are exclusively NR1/NR2B diheteromers, whilst postsynaptically they are probably a mixture of NR1/NR2A, NR1/NR2B diheteromers and NR1/NR2A/NR2B triheteromeric receptors.

Muscarinic presynaptic modulation in GABAergic pallidal synapses of the rat

2015 ◽  
Vol 113 (3) ◽  
pp. 796-807 ◽  
Author(s):  
Ricardo Hernández-Martínez ◽  
José J. Aceves ◽  
Pavel E. Rueda-Orozco ◽  
Teresa Hernández-Flores ◽  
Omar Hernández-González ◽  
...  
Keyword(s):  
Receptor Agonist ◽  
Projection Neurons ◽  
Quantal Content ◽  
Short Term ◽  
Paired Pulse ◽  
Short Term Plasticity ◽  
Striatal Projection Neurons ◽  
Muscarinic Cholinergic ◽  
Muscarinic Modulation

The external globus pallidus (GPe) is central for basal ganglia processing. It expresses muscarinic cholinergic receptors and receives cholinergic afferents from the pedunculopontine nuclei (PPN) and other regions. The role of these receptors and afferents is unknown. Muscarinic M1-type receptors are expressed by synapses from striatal projection neurons (SPNs). Because axons from SPNs project to the GPe, one hypothesis is that striatopallidal GABAergic terminals may be modulated by M1 receptors. Alternatively, some M1 receptors may be postsynaptic in some pallidal neurons. Evidence of muscarinic modulation in any of these elements would suggest that cholinergic afferents from the PPN, or other sources, could modulate the function of the GPe. In this study, we show this evidence using striatopallidal slice preparations: after field stimulation in the striatum, the cholinergic muscarinic receptor agonist muscarine significantly reduced the amplitude of inhibitory postsynaptic currents (IPSCs) from synapses that exhibited short-term synaptic facilitation. This inhibition was associated with significant increases in paired-pulse facilitation, and quantal content was proportional to IPSC amplitude. These actions were blocked by atropine, pirenzepine, and mamba toxin-7, suggesting that receptors involved were M1. In addition, we found that some pallidal neurons have functional postsynaptic M1 receptors. Moreover, some evoked IPSCs exhibited short-term depression and a different kind of modulation: they were indirectly modulated by muscarine via the activation of presynaptic cannabinoid CB1 receptors. Thus pallidal synapses presenting distinct forms of short-term plasticity were modulated differently.

scholarly journals 1M0900 The role of Ca^ concentration for short term plasticity (augmentation, potentiation)

2002 ◽  
Vol 42 (supplement2) ◽  
pp. S73
Author(s):  
H. Yamamoto ◽  
M. Murase ◽  
N. Suzuki
Keyword(s):  
Short Term ◽  
Short Term Plasticity

scholarly journals Molecular Mechanisms of Oxytocin Signaling at the Synaptic Connection

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Jan Bakos ◽  
Annamaria Srancikova ◽  
Tomas Havranek ◽  
Zuzana Bacova
Keyword(s):  
Neurodevelopmental Disorders ◽  
Molecular Mechanisms ◽  
Neuronal Excitability ◽  
Molecular Level ◽  
Short Term ◽  
Oxytocin Receptors ◽  
Potential Therapeutic Intervention ◽  
Early Alteration

Aberrant regulation of oxytocin signaling is associated with the etiology of neurodevelopmental disorders. Synaptic dysfunctions in neurodevelopmental disorders are becoming increasingly known, and their pathogenic mechanisms could be a target of potential therapeutic intervention. Therefore, it is important to pay attention to the role of oxytocin and its receptor in synapse structure, function, and neuron connectivity. An early alteration in oxytocin signaling may disturb neuronal maturation and may have short-term and long-term pathological consequences. At the molecular level, neurodevelopmental disorders include alterations in cytoskeletal rearrangement and neuritogenesis resulting in a diversity of synaptopathies. The presence of oxytocin receptors in the presynaptic and postsynaptic membranes and the direct effects of oxytocin on neuronal excitability by regulating the activity of ion channels in the cell membrane implicate that alterations in oxytocin signaling could be involved in synaptopathies. The ability of oxytocin to modulate neurogenesis, synaptic plasticity, and certain parameters of cytoskeletal arrangement is discussed in the present review.

scholarly journals Role of Thalamic Projection in NMDA Receptor-Induced Disruption of Cortical Slow Oscillation and Short-Term Plasticity

2011 ◽  
Vol 2 ◽  
Author(s):  
Tamás Kiss ◽  
William E. Hoffmann ◽  
Liam Scott ◽  
Thomas T. Kawabe ◽  
Anthony J. Milici ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Slow Oscillation ◽  
Short Term ◽  
Short Term Plasticity

Distinct Transmitter Release Properties Determine Differences in Short-Term Plasticity at Functional and Silent Synapses

2006 ◽  
Vol 95 (5) ◽  
pp. 3024-3034 ◽  
Author(s):  
Carolina Cabezas ◽  
Washington Buño
Keyword(s):  
Transmitter Release ◽  
Molecular Mechanisms ◽  
Long Term Potentiation ◽  
Lower Percentage ◽  
Functional Importance ◽  
Short Term ◽  
Short Term Plasticity ◽  
Silent Synapses ◽  
Term Potentiation

Recent evidence suggests that functional and silent synapses are not only postsynaptically different but also presynaptically distinct. The presynaptic differences may be of functional importance in memory formation because a proposed mechanism for long-term potentiation is the conversion of silent synapses into functional ones. However, there is little direct experimentally evidence of these differences. We have investigated the transmitter release properties of functional and silent Schaffer collateral synapses and show that on the average functional synapses displayed a lower percentage of failures and higher excitatory postsynaptic current (EPSC) amplitudes than silent synapses at +60 mV. Moreover, functional but not silent synapses show paired-pulse facilitation (PPF) at +60 mV and thus presynaptic short-term plasticity will be distinct in the two types of synapse. We examined whether intraterminal endoplasmic reticulum Ca2+ stores influenced the release properties of these synapses. Ryanodine (100 μM) and thapsigargin (1 μM) increased the percentage of failures and decreased both the EPSC amplitude and PPF in functional synapses. Caffeine (10 mM) had the opposite effects. In contrast, silent synapses were insensitive to both ryanodine and caffeine. Hence we have identified differences in the release properties of functional and silent synapses, suggesting that synaptic terminals of functional synapses express regulatory molecular mechanisms that are absent in silent synapses.

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