シナプス前受容体、シナプス前レセプター

WordNet

a cellular structure that is postulated to exist in order to mediate between a chemical agent that acts on nervous tissue and the physiological response

PrepTutorEJDIC

=sense organ / 受信装置

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1. インスリン受容体の構造および機能 structure and function of the insulin receptor
2. 免疫不全症を引き起こすCD3／T細胞受容体複合体疾患 cd3 t cell receptor complex disorders causing immunodeficiency
3. 成人における肥満：薬物療法 obesity in adults drug therapy
4. T細胞受容体の遺伝学 t cell receptor genetics
5. T細胞受容体シグナル伝達 t cell receptor signaling

English Journal

Kinetics of neurotransmitter release in neuromuscular synapses of newborn and adult rats.

Khuzakhmetova V1, Samigullin D1, Nurullin L1, Vyskočil F2, Nikolsky E3, Bukharaeva E4.Author information 1Kazan Institute of Biochemistry and Biophysics Kazan Scientific Center of the Russian Academy of Sciences, Post Box 30, 420111 Kazan, Russia.2Institute of Physiology, Academy of Sciences of the Czech Republic, Videnska 1083, 14200 Prague, Czech Republic; Department of Physiology, Faculty of Sciences, Charles University, Vinicna 7, Prague, Czech Republic.3Kazan Institute of Biochemistry and Biophysics Kazan Scientific Center of the Russian Academy of Sciences, Post Box 30, 420111 Kazan, Russia; Kazan State Medical University, Butlerov st. 49, 420012 Kazan, Russia; Kazan Federal University, Kremlyovskaya st. 18, 420008 Kazan, Russia.4Kazan Institute of Biochemistry and Biophysics Kazan Scientific Center of the Russian Academy of Sciences, Post Box 30, 420111 Kazan, Russia; Kazan State Medical University, Butlerov st. 49, 420012 Kazan, Russia; Kazan Federal University, Kremlyovskaya st. 18, 420008 Kazan, Russia. Electronic address: elbukhara@gmail.com.AbstractThe kinetics of the phasic synchronous and delayed asynchronous release of acetylcholine quanta was studied at the neuromuscular junctions of aging rats from infant to mature animals at various frequencies of rhythmic stimulation of the motor nerve. We found that in infants 6 (P6) and 10 (P10) days after birth a strongly asynchronous phase of quantal release was observed, along with a reduced number of quanta compared to the synapses of adults. The rise time and decay of uni-quantal end-plate currents were significantly longer in infant synapses. The presynaptic immunostaining revealed that the area of the synapses in infants was significantly (up to six times) smaller than in mature junctions. The intensity of delayed asynchronous release in infants increased with the frequency of stimulation more than in adults. A blockade of the ryanodine receptors, which can contribute to the formation of delayed asynchronous release, had no effect on the kinetics of delayed secretion in the infants unlike synapses of adults. Therefore, high degree of asynchrony of quantal release in infants is not associated with the activity of ryanodine receptors and with the liberation of calcium ions from intracellular calcium stores.
International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience.Int J Dev Neurosci.2014 May;34:9-18. doi: 10.1016/j.ijdevneu.2013.12.010. Epub 2014 Jan 9.
The kinetics of the phasic synchronous and delayed asynchronous release of acetylcholine quanta was studied at the neuromuscular junctions of aging rats from infant to mature animals at various frequencies of rhythmic stimulation of the motor nerve. We found that in infants 6 (P6) and 10 (P10) days
PMID 24412779

Presynaptic membrane receptors in acetylcholine release modulation in the neuromuscular synapse.

Tomàs J1, Santafé MM, Garcia N, Lanuza MA, Tomàs M, Besalduch N, Obis T, Priego M, Hurtado E.Author information 1Unitat d'Histologia i Neurobiologia (UHN), Facultat de Medicina i Ciències de la Salut, Universitat Rovira i Virgili, Reus, Spain.AbstractOver the past few years, we have studied, in the mammalian neuromuscular junction (NMJ), the local involvement in transmitter release of the presynaptic muscarinic ACh autoreceptors (mAChRs), purinergic adenosine autoreceptors (P1Rs), and trophic factor receptors (TFRs; for neurotrophins and trophic cytokines) during development and in the adult. At any given moment, the way in which a synapse works is largely the logical outcome of the confluence of these (and other) metabotropic signalling pathways on intracellular kinases, which phosphorylate protein targets and materialize adaptive changes. We propose an integrated interpretation of the complementary function of these receptors in the adult NMJ. The activity of a given receptor group can modulate a given combination of spontaneous, evoked, and activity-dependent release characteristics. For instance, P1Rs can conserve resources by limiting spontaneous quantal leak of ACh (an A1 R action) and protect synapse function, because stimulation with adenosine reduces the magnitude of depression during repetitive activity. The overall outcome of the mAChRs seems to contribute to upkeep of spontaneous quantal output of ACh, save synapse function by decreasing the extent of evoked release (mainly an M2 action), and reduce depression. We have also identified several links among P1Rs, mAChRs, and TFRs. We found a close dependence between mAChR and some TFRs and observed that the muscarinic group has to operate correctly if the tropomyosin-related kinase B receptor (trkB) is also to operate correctly, and vice versa. Likewise, the functional integrity of mAChRs depends on P1Rs operating normally. © 2014 Wiley Periodicals, Inc.
Journal of neuroscience research.J Neurosci Res.2014 May;92(5):543-54. doi: 10.1002/jnr.23346. Epub 2014 Jan 27.
Over the past few years, we have studied, in the mammalian neuromuscular junction (NMJ), the local involvement in transmitter release of the presynaptic muscarinic ACh autoreceptors (mAChRs), purinergic adenosine autoreceptors (P1Rs), and trophic factor receptors (TFRs; for neurotrophins and trophic
PMID 24464361

Enhanced mossy fiber sprouting and synapse formation in organotypic hippocampal cultures following transient domoic Acid excitotoxicity.

Pérez-Gómez A1, Tasker RA.Author information 1Department of Biomedical Sciences, University of Prince Edward Island, 550 University Avenue, Charlottetown, PE, C1A 4P3, Canada.AbstractWe have previously reported evidence of BDNF upregulation and increased neurogenesis in rat organotypic hippocampal slice cultures (OHSC) after a transient excitotoxic injury to the hippocampal CA1 area induced by low concentrations of the AMPA/kainate receptor agonist domoic acid (DOM). The changes observed in OHSC were consistent with observations in vivo, where low concentrations of DOM administered to rats during perinatal development caused increased BDNF and TrkB expression in the resulting adult animals. The in vivo low dose-DOM treatment also results in permanent alterations in hippocampal structure and function, including abnormal formation of dentate granule cell axons projecting to area CA3 (mossy fiber sprouting). Our objective in the current study is to determine if low concentrations of DOM induce mossy fiber sprouting and/or synaptogenesis in OHSC in order to facilitate future studies on the mechanisms of structural hippocampal plasticity induced by DOM. We report herein that application of a low concentration of DOM (2 μM) for 24 h followed by recovery induced a significant increase in the expression of the mossy fiber marker ZnT3 that progressed over time in culture. The DOM insult (2 μM, 24 h) also resulted in a significant upregulation of both the presynaptic marker synaptophysin and the postsynaptic marker PSD-95. All of the observed effects were fully antagonized by co-administration of the AMPA/kainate antagonists CNQX or NBQX but only partly by the NMDA antagonist CPP and not by the calcium channel blocker nifedipine. We conclude that exposure of OHSC to concentrations of DOM below those required to induce permanent neurotoxicity can induce a progressive change in hippocampal structure that can effectively model DOM effects in vivo.
Neurotoxicity research.Neurotox Res.2014 May;25(4):402-10. doi: 10.1007/s12640-013-9450-z. Epub 2013 Dec 18.
We have previously reported evidence of BDNF upregulation and increased neurogenesis in rat organotypic hippocampal slice cultures (OHSC) after a transient excitotoxic injury to the hippocampal CA1 area induced by low concentrations of the AMPA/kainate receptor agonist domoic acid (DOM). The changes
PMID 24347374

Japanese Journal

Endocannabinoid-mediated retrograde modulation of synaptic transmission

Ohno-Shosaku Takako,Kano Masanobu
Current Opinion in Neurobiology 29, 1-8, 2014-12
… Upon postsynaptic activation, 2-AG is released immediately after de novo synthesis, activates presynaptic CB1 cannabinoid receptors, and transiently suppresses neurotransmitter release. … When CB1 receptor activation is combined with some other factors such as presynaptic activity, the suppression is converted to a long-lasting form. …
NAID 120005435504

Presynaptic Inhibitory Effects of Fluvoxamine, a Selective Serotonin Reuptake Inhibitor, on Nociceptive Excitatory Synaptic Transmission in Spinal Superficial Dorsal Horn Neurons of Adult Mice

Tomoyose Orie,Kodama Daisuke,Ono Hideki,Tanabe Mitsuo
Journal of Pharmacological Sciences 126(2), 136-145, 2014
… Fluvoxamine (10 – 100 μM) concentration-dependently suppressed both monosynaptic A-fiber- and C-fiber-mediated EPSCs, which were attenuated by the selective 5-HT1A receptor antagonist WAY100635. … In the presence of the selective 5-HT3 receptor antagonist tropisetron, fluvoxamine hardly suppressed A-fiber-mediated EPSCs, whereas its inhibitory effect on C-fiber-mediated EPSCs was not affected. …
NAID 130004690916

Control of synaptic function by endocannabinoid-mediated retrograde signaling

KANO Masanobu
Proceedings of the Japan Academy, Series B 90(7), 235-250, 2014
… The released 2-AG then acts retrogradely onto presynaptic cannabinoid CB1 receptors and induces suppression of neurotransmitter release either transiently or persistently. …
NAID 130004678273