 |
||||
|
||||
|
||||
|
||||
.gif?ad=17923&adview=true)
Previous Article | Next Article
The Journal of Neuroscience, March 15, 2001, 21(6):1911-1922
Differential Regulation of Transmitter Release by Presynaptic and Glial Ca2+ Internal Stores at the Neuromuscular Synapse
Annie Castonguay and Richard Robitaille Centre de Recherche en Sciences Neurologiques and Département de Physiologie, Université de Montréal, Montréal, Canada H3C 3J7
The differential regulation of synaptic transmission by internal Ca2+ stores of presynaptic terminals and perisynaptic Schwann cells (PSCs) was studied at the frog neuromuscular junction. Thapsigargin (tg), an inhibitor of Ca2+-ATPase pumps of internal stores, caused a transient Ca2+ elevation in PSCs, whereas it had no effect on Ca2+ stores of presynaptic terminals at rest. Tg prolonged presynaptic Ca2+ responses evoked by single action potentials with no detectable increase in the resting Ca2+ level in nerve terminals. However, Ca2+ accumulation was observed during high frequency stimulation. Tg induced a rapid rise in endplate potential (EPP) amplitude, accompanied by a delayed and transient increase. The effects appeared presynaptic, as suggested by the lack of effects of tg on the amplitude and time course of miniature EPPs (MEPPs). However, MEPP frequency was increased when preparations were stimulated tonically (0.2 Hz). The delayed and transient increase in EPP amplitude was occluded by injections of the Ca2+ chelator BAPTA into PSCs before tg application, whereas a rise in intracellular Ca2+ in PSCs induced by inositol 1,4,5-triphosphate (IP3) injections potentiated transmitter release. Furthermore, increased Ca2+ buffering capacity after BAPTA injection in PSCs resulted in a more pronounced synaptic depression induced by high frequency stimulation of the motor nerve (10 Hz/80 sec). It is concluded that presynaptic Ca2+ stores act as a Ca2+ clearance mechanism to limit the duration of transmitter release, whereas Ca2+ release from glial stores initiates Ca2+-dependent potentiation of synaptic transmission.
Key words: perisynaptic Schwann cells; ATPase pump; calcium; frog neuromuscular junction; transmitter release; synaptic transmission; synapse-glia interactions; IP3
Copyright © 2001 Society for Neuroscience 0270-6474/01/2161911-12$05.00/0
This article has been cited by other articles:
G. Cao and C.-P. Ko
Schwann Cell-Derived Factors Modulate Synaptic Activities at Developing Neuromuscular Synapses
J. Neurosci., June 20, 2007; 27(25): 6712 - 6722.
[Abstract] [Full Text] [PDF]
K. Reiss, T. Maretzky, I. G. Haas, M. Schulte, A. Ludwig, M. Frank, and P. Saftig
Regulated ADAM10-dependent Ectodomain Shedding of {gamma}-Protocadherin C3 Modulates Cell-Cell Adhesion
J. Biol. Chem., August 4, 2006; 281(31): 21735 - 21744.
[Abstract] [Full Text] [PDF]
Z. Feng, S. Koirala, and C.-P. Ko
Synapse-Glia Interactions at the Vertebrate Neuromuscular Junction
Neuroscientist, October 1, 2005; 11(5): 503 - 513.
[Abstract] [PDF]
Y. Q. Lin and M. R. Bennett
Varicosity-Schwann Cell Interactions Mediated by ATP in the Mouse Vas Deferens
J Neurophysiol, May 1, 2005; 93(5): 2787 - 2796.
[Abstract] [Full Text] [PDF]
A. Verkhratsky
Physiology and Pathophysiology of the Calcium Store in the Endoplasmic Reticulum of Neurons
Physiol Rev, January 1, 2005; 85(1): 201 - 279.
[Abstract] [Full Text] [PDF]
G. Corfas, M. O. Velardez, C.-P. Ko, N. Ratner, and E. Peles
Mechanisms and Roles of Axon-Schwann Cell Interactions
J. Neurosci., October 20, 2004; 24(42): 9250 - 9260.
[Full Text] [PDF]
V. De Crescenzo, R. ZhuGe, C. Velazquez-Marrero, L. M. Lifshitz, E. Custer, J. Carmichael, F. A. Lai, R. A. Tuft, K. E. Fogarty, J. R. Lemos, et al.
Ca2+ Syntillas, Miniature Ca2+ Release Events in Terminals of Hypothalamic Neurons, Are Increased in Frequency by Depolarization in the Absence of Ca2+ Influx
J. Neurosci., February 4, 2004; 24(5): 1226 - 1235.
[Abstract] [Full Text] [PDF]
J. A. Powell, J. Molgo, D. S. Adams, C. Colasante, A. Williams, M. Bohlen, and E. Jaimovich
IP3 Receptors and Associated Ca2+ Signals Localize to Satellite Cells and to Components of the Neuromuscular Junction in Skeletal Muscle
J. Neurosci., September 10, 2003; 23(23): 8185 - 8192.
[Abstract] [Full Text] [PDF]
J. Piriz, M. D. Rosato Siri, R. Pagani, and O. D. Uchitel
Nifedipine-Mediated Mobilization of Intracellular Calcium Stores Increases Spontaneous Neurotransmitter Release at Neonatal Rat Motor Nerve Terminals
J. Pharmacol. Exp. Ther., August 1, 2003; 306(2): 658 - 663.
[Abstract] [Full Text] [PDF]
D. S. Auld and R. Robitaille
Perisynaptic Schwann Cells at the Neuromuscular Junction: Nerve- and Activity-Dependent Contributions to Synaptic Efficacy, Plasticity, and Reinnervation
Neuroscientist, April 1, 2003; 9(2): 144 - 157.
[Abstract] [PDF]
E. A. Newman
Glial Cell Inhibition of Neurons by Release of ATP
J. Neurosci., March 1, 2003; 23(5): 1659 - 1666.
[Abstract] [Full Text] [PDF]
R. D. Fields and B. Stevens-Graham
NEUROSCIENCE: New Insights into Neuron-Glia Communication
Science, October 18, 2002; 298(5593): 556 - 562.
[Abstract] [Full Text] [PDF]
A. G. Carter, K. E. Vogt, K. A. Foster, and W. G. Regehr
Assessing the Role of Calcium-Induced Calcium Release in Short-Term Presynaptic Plasticity at Excitatory Central Synapses
J. Neurosci., January 1, 2002; 22(1): 21 - 28.
[Abstract] [Full Text] [PDF]
J.-F. Yang, G. Cao, S. Koirala, L. V. Reddy, and C.-P. Ko
Schwann Cells Express Active Agrin and Enhance Aggregation of Acetylcholine Receptors on Muscle Fibers
J. Neurosci., December 15, 2001; 21(24): 9572 - 9584.
[Abstract] [Full Text] [PDF]
D. Rochon, I. Rousse, and R. Robitaille
Synapse-Glia Interactions at the Mammalian Neuromuscular Junction
J. Neurosci., June 1, 2001; 21(11): 3819 - 3829.
[Abstract] [Full Text] [PDF]
|
|
|
|
 |
|