Elizabeth A Jonas MD
Associate Professor of Medicine (Endocrinology) and of Neurobiology
Mitochondrial ion channel; regulation of apoptosis; control of the strength of synaptic transmission in the nervous system
- Role of Bcl-xL in brain ischemia
- Role of Bcl-xL in synaptic plasticity
- Role of Bcl-xL in neuronal metabolism
- Role of mitochondrial bioenergetics in Parkinson's Disease
Some of the features of neuronal synaptic transmission that can be modified over the short and long term include changes in presynaptic calcium levels, changes in vesicle numbers and probability of release, and alterations in postsynaptic receptor numbers and function. Such variations account in part for the synaptic plasticity that may underlie learning and memory. Alterations in levels of activity at the synapse require increased energy, and therefore mitochondria could influence synaptic events by regulating the production or release of ATP, or by buffering and re-releasing calcium during vesicle fusion and recycling. BCL-2 family proteins, by their actions at mitochondrial membranes, normally play an important role in cell death at the soma, but can also strengthen or weaken synaptic connections.
Thus the actions of mitochondria at synaptic sites position these organelles to influence physiological and pathological changes in the brain. In neurodegenerative diseases, proteins that control mitochondrial ion channel activity may be key in deciding whether a synapse will live or die, and eventually, after the loss of many synaptic connections, whether a neuron will survive or undergo untimely death.