The Journal of Neuroscience, December 15, 2002, 22(24):10524-10528
BRIEF COMMUNICATION
Presynaptic Ca2+ Entry Is Unchanged during
Hippocampal Mossy Fiber Long-Term Potentiation
Haruyuki
Kamiya1, 2,
Kazumasa
Umeda1, 3,
Seiji
Ozawa2, 4, and
Toshiya
Manabe1, 5
1 Division of Cell Biology and Neurophysiology,
Department of Neuroscience, Faculty of Medicine, Kobe University, Kobe,
Hyogo 650-0017, Japan, 2 Department of Physiology, Gunma
University School of Medicine, Maebashi, Gunma 371-8511, Japan,
3 Department of Applied Biology, Kyoto Institute of
Technology, Kyoto 606-8585, Japan, 4 Core Research for
Evolutional Science and Technology, Japan Science and Technology
Corporation, Kawaguchi, Saitama 332-0012, Japan, and
5 Division of Neuronal Network, Department of Basic Medical
Sciences, Institute of Medical Science, University of Tokyo, Tokyo
108-8639, Japan
The hippocampal mossy fiber (MF)-CA3 synapse exhibits
NMDA receptor-independent long-term potentiation (LTP), which is
expressed by presynaptic mechanisms leading to persistent enhancement
of transmitter release. Recent studies have identified several
molecules that may play an important role in MF-LTP. These include
Rab3A, RIM1
, kainate autoreceptor, and
hyperpolarization-activated cation channel
(Ih). However, the precise cellular
expression mechanism remains to be determined because some studies
noticed essential roles of release machinery molecules, whereas others
suggested modulation of the ionotropic processes affecting
Ca2+ entry into the presynaptic terminals. Using
fluorescence recordings of presynaptic Ca2+ in
hippocampal slices, here we demonstrated that MF-LTP is not accompanied
by an increase in presynaptic Ca2+ influx during an
action potential. Whole-cell recordings from CA3 neurons revealed
long-lasting increases in mean frequency, but not mean amplitude, of
miniature EPSCs after the high-frequency stimulation of MFs.
These data indicate that the presynaptic expression mechanisms
responsible for enhanced transmitter release during MF-LTP involve
persistent modification of presynaptic molecular targets residing
downstream of Ca2+ entry.
Key words:
cAMP; hippocampus; long-term potentiation; mossy fiber; presynaptic Ca2+ influx; transmitter release
Copyright © 2002 Society for Neuroscience 0270-6474/02/222410524-05$05.00/0