MI Visit the ASPET Website
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Molecular Interventions 6:208-222, (2006)
© American Society for Pharmacology and Experimental Therapeutics
10.1124/mi.6.4.7
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jonas, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jonas, E.
Review

BCL-xL Regulates Synaptic Plasticity

Elizabeth Jonas

Yale University School of Medicine, Section of Endocrinology, Department of Internal Medicine, 333 Cedar Street, PO Box 208020, New Haven, CT 06520-8020


Formula

Mitochondria are the predominant organelle within many presynaptic terminals. During times of high synaptic activity, they affect intracellular calcium homeostasis and provide the energy needed for synaptic vesicle recycling and for the continued operation of membrane ion pumps. Recent discoveries have altered our ideas about the role of mitochondria in the synapse. Mitochondrial localization, morphology, and docking at synaptic sites may indeed alter the kinetics of transmitter release and calcium homeostasis in the presynaptic terminal. In addition, the mitochondrial ion channel BCL-xL, known as a protector against programmed cell death, regulates mitochondrial membrane conductance and bioenergetics in the synapse and can thereby alter synaptic transmitter release and the recycling of pools of synaptic vesicles. BCL-xL, therefore, not only affects the life and death of the cell soma, but its actions in the synapse may underlie the regulation of basic synaptic processes that subtend learning, memory and synaptic development.




This article has been cited by other articles:


Home page
 Proc. Natl. Acad. Sci. USAHome page
T. Miyawaki, T. Mashiko, D. Ofengeim, R. J. Flannery, K.-M. Noh, S. Fujisawa, L. Bonanni, M. V. L. Bennett, R. S. Zukin, and E. A. Jonas
Ischemic preconditioning blocks BAD translocation, Bcl-xL cleavage, and large channel activity in mitochondria of postischemic hippocampal neurons
PNAS, March 25, 2008; 105(12): 4892 - 4897.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
H. Li, Y. Chen, A. F. Jones, R. H. Sanger, L. P. Collis, R. Flannery, E. C. McNay, T. Yu, R. Schwarzenbacher, B. Bossy, et al.
Bcl-xL induces Drp1-dependent synapse formation in cultured hippocampal neurons
PNAS, February 12, 2008; 105(6): 2169 - 2174.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
C. A. Hoeffer, A. Dey, N. Sachan, H. Wong, R. J. Patterson, J. M. Shelton, J. A. Richardson, E. Klann, and B. A. Rothermel
The Down Syndrome Critical Region Protein RCAN1 Regulates Long-Term Potentiation and Memory via Inhibition of Phosphatase Signaling
J. Neurosci., November 28, 2007; 27(48): 13161 - 13172.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ASPET Journals Pharmacological Reviews Drug Metabolism and Disposition
Molecular Interventions Molecular Pharmacology J Pharmacology and Exp Therapeutics
Copyright © 2006 by the American Society for Pharmacology and Experimental Therapeutics.