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  • English  (4)
  • 1995-1999  (4)
  • Linguistics  (4)
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  • English  (4)
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  • 1995-1999  (4)
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  • 1
    Online Resource
    Online Resource
    American Association for the Advancement of Science (AAAS) ; 1996
    In:  Science Vol. 272, No. 5266 ( 1996-05-31), p. 1356-1357
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 272, No. 5266 ( 1996-05-31), p. 1356-1357
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    RVK:
    RVK:
    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 1996
    detail.hit.zdb_id: 128410-1
    detail.hit.zdb_id: 2066996-3
    detail.hit.zdb_id: 2060783-0
    SSG: 11
    Location Call Number Limitation Availability
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  • 2
    Online Resource
    Online Resource
    Society for Neuroscience ; 1998
    In:  The Journal of Neuroscience Vol. 18, No. 23 ( 1998-12-01), p. 9954-9961
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 18, No. 23 ( 1998-12-01), p. 9954-9961
    Abstract: The activation of autoreceptors is known to be important in the modulation of presynaptic transmitter secretion in peripheral and central neurons. Using whole-cell recordings made from the free growth cone of myocyte-contact motoneurons of Xenopus cell cultures, we have observed spontaneous nerve terminal currents (NTCs). These spontaneous NTCs are blocked by d-tubocurarine (d-TC) and α-bungarotoxin (α-BuTx), indicating that endogenously released acetylcholine (ACh) can produce substantial membrane depolarization in the nerve terminals. Local application of NMDA to the growth cone increased the frequency of spontaneous NTCs. When the electrical stimulations were applied at the soma to initiate evoked-release of ACh, evoked ACh-induced potentials were recorded in the nerve terminals, which were inhibited by d-TC and hexamethonium but not by atropine. Replacement of normal Ringer’s solution with high-Mg 2+ , low-Ca 2+ solution also reversibly inhibited evoked ACh-induced potentials. The possible regulatory role of presynaptic nicotinic autoreceptors on the synaptic transmission was also examined. When the innervated myocyte was whole-cell voltage-clamped to record synaptic currents, application of hexamethonium inhibited the amplitude of evoked synaptic currents at a higher degree than that of iontophoretic ACh-induced currents. Furthermore, hexamethonium markedly reduced the frequency of spontaneous synaptic currents at high-activity synapses. Pretreatment of neurons with α-BuTx also inhibited the evoked synaptic currents in manipulated synapses. These results suggest that ACh released spontaneously or by electrical stimulation may act on the presynaptic nicotinic autoreceptors of the same nerve terminals to produce membrane potential change and to regulate synaptic transmission.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1998
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Society for Neuroscience ; 1997
    In:  The Journal of Neuroscience Vol. 17, No. 7 ( 1997-04-01), p. 2459-2468
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 17, No. 7 ( 1997-04-01), p. 2459-2468
    Abstract: Neurotrophic factors derived from postsynaptic muscle cells may play important roles in the development of presynaptic neuronal functions. In 3-d-old Xenopus nerve–muscle cultures, embryonic spinal neurons that had made natural contact with co-cultured myocytes exhibited spontaneous release of larger packets of acetylcholine (ACh) quanta than those released by the isolated neurons having no contact with any myocyte. Treatment of isolated neurons with neurotrophin-3 (NT-3) for 2 d increased the average sizes of quantal ACh packets at newly formed nerve–muscle synapses, whereas treatment with antibody against NT-3 or with K252a, a specific inhibitor of tyrosine kinase receptors, decreased the quantal size at existing synapses, which suggests that NT-3 supplied by the postsynaptic muscle cell may be responsible for the development and maintenance of the quantal packets. The muscle effect seems to depend on synaptic activities mediated by postsynaptic ACh receptor channels, because chronic treatment of the culture with d -tubocurarine ( d -Tc) for 2 d resulted in a marked reduction of the quantal sizes, when assayed after extensive washing of the culture with Ringer’s solution. The curare treatment did not affect the postsynaptic ACh receptor sensitivity, because iontophoretically applied ACh induced current responses similar to those of control. Finally, co-treatment of the culture with NT-3 and d -Tc reversed the effect of d -Tc on the quantal size, and this reversal effect was abolished when K252a was also applied concomitantly. Our results suggest that muscle-derived NT-3 participates in the maturation of normal transmitter packets in developing neurons, and the secretion of NT-3 depends on spontaneous synaptic activity.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1997
    detail.hit.zdb_id: 1475274-8
    SSG: 12
    Location Call Number Limitation Availability
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  • 4
    Online Resource
    Online Resource
    Society for Neuroscience ; 1998
    In:  The Journal of Neuroscience Vol. 18, No. 8 ( 1998-04-15), p. 2982-2990
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 18, No. 8 ( 1998-04-15), p. 2982-2990
    Abstract: NMDA receptors play important roles in synaptic plasticity and neuronal development. The functions of NMDA receptors are modulated by many endogenous substances, such as external pH (pH e ), as well as second messenger systems. In the present study, the nerve–muscle cocultures of Xenopus embryos were used to investigate the effects of both external and intracellular pH (pH i ) changes on the functional responses of presynaptic NMDA receptors. Spontaneous synaptic currents (SSCs) were recorded from innervated myocyte using whole-cell recordings. Local perfusion of NMDA at synaptic regions increased the SSC frequency via the activation of presynaptic NMDA receptors. A decrease in pH e from 7.6 to 6.6 reduced NMDA responses to 23% of the control, and an increase in pH e from 7.6 to 8.6 potentiated the NMDA responses in increasing SSC frequency. The effect of NMDA on intracellular Ca 2+ concentration ([Ca 2+ ] i ) was also affected by pH e changes: external acidification inhibited and alkalinization potentiated [Ca 2+ ] i increases induced by NMDA. Intracellular pH changes of single soma were measured by ratio fluorometric method using 2,7-bis (carboxyethyl)-5,6-carboxyfluorescein (BCECF). Cytosolic acidification was used in which NaCl in Ringer’s solution was replaced with weak organic acids. Acetate and propionate but not methylsulfate substitution caused intracellular acidification and potentiated NMDA responses in increasing SSC frequency, intracellular free Ca 2+ concentration, and NMDA-induced currents. On the other hand, cytosolic alkalinization with NH 4 Cl did not significantly affect these NMDA responses. These results suggest that the functions of NMDA receptors are modulated by both pH e and pH i changes, which may occur in some physiological or pathological conditions.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1998
    detail.hit.zdb_id: 1475274-8
    SSG: 12
    Location Call Number Limitation Availability
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