|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||
Received December 18, 2001
Accepted after revision April 23, 2002
1 Department of Integrative Medical Biology, Section for Physiology, Umea University, S-901 87 Umea, Sweden and Laboratory of Ionic Channels of Cell Membranes, Institute of Cytology, Russian Academy of Sciences, St Petersburg 194064, Russia
2 Department of Integrative Medical Biology, Section for Physiology, Umea University, S-901 87 Umea, Sweden
* To whom correspondence should be addressed. E-mail: staffan.johansson{at}physiol.umu.se.
Calcium influx into the presynaptic nerve terminal is well established as a trigger signal for transmitter release by exocytosis. By studying dissociated preoptic neurons with functional adhering nerve terminals, we here show that presynaptic Ca2+ influx plays dual and opposing roles in the control of spontaneous transmitter release. Thus, application of various Ca2+ channel blockers paradoxically increased the frequency of spontaneous (miniature) inhibitory GABA-mediated postsynaptic currents (mIPSCs). Similar effects on mIPSC frequency were recorded upon washout of Cd2+ or EGTA from the external solution. The results are explained by a model with parallel Ca2+ influx through channels coupled to the exocytotic machinery and through channels coupled to Ca2+-activated K+ channels at a distance from the release site.
This article has been cited by other articles:
![]() |
J.-H. Ye, F. Wang, K. Krnjevic, W. Wang, Z.-G. Xiong, and J. Zhang Presynaptic Glycine Receptors on GABAergic Terminals Facilitate Discharge of Dopaminergic Neurons in Ventral Tegmental Area J. Neurosci., October 13, 2004; 24(41): 8961 - 8974. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Hirasawa and Q. J. Pittman From the Cover: Nifedipine facilitates neurotransmitter release independently of calcium channels PNAS, May 13, 2003; 100(10): 6139 - 6144. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |