Related Experiment Video
Updated: Jul 20, 2026

Assessment of Long-term Depression Induction in Adult Cerebellar Slices
Published on: October 16, 2019
BCL-xL regulates synaptic plasticity
1Yale University School of Medicine, Section of Endocrinology, Department of Internal Medicine, 333 Cedar Street, PO Box 208020, New Haven, CT 06520-8020, USA. elizabeth.jonas@yale.edu
Abstract:
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.
Related Concept Videos
Long-term Depression
Calcium Ion Concentration Mechanism
If over time, all...
Long-term Depression
Long-term Potentiation
Long-term Potentiation
Hebbian LTP
LTP can occur when presynaptic neurons...
Neuroplasticity
Chemical Synapses
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is...

