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Sr2+-dependent asynchronous evoked transmission at rat striatal inhibitory synapses in vitro
1Department of Physiology, University of Munich, Pettenkoferstrasse 12, 80336 Munchen, Germany.
The Journal of Physiology
|December 16, 1998
Summary
Strontium (Sr2+) ions, unlike calcium (Ca2+), cause asynchronous neurotransmitter release at inhibitory synapses by interacting differently with intracellular components. This suggests less efficient intraterminal buffering of Sr2+ leads to synaptic desynchronization.
Area of Science:
- Neuroscience
- Cell Biology
- Synaptic Transmission
Background:
- Calcium ions (Ca2+) are critical for neurotransmitter release.
- Strontium ions (Sr2+) can substitute for Ca2+ in some biological processes.
- Understanding ion-specific mechanisms of synaptic release is key to neuroscience.
Purpose of the Study:
- To investigate the distinct effects of Sr2+ versus Ca2+ on inhibitory synaptic transmission.
- To elucidate the underlying mechanisms of Sr2+-induced asynchronous neurotransmitter release.
Main Methods:
- Utilized cell culture of striatal inhibitory synapses.
- Replaced extracellular Ca2+ with Sr2+ to observe synaptic current changes.
- Employed rapid solution exchange and intracellular Ca2+-chelators (BAPTA AM, EGTA AM).
Main Results:
- Sr2+ desynchronized inhibitory postsynaptic currents (IPSCs), reducing peak amplitude and causing late, asynchronous release.
- Late release was independent of continuous Sr2+ influx, indicating intracellular interactions.
- Intracellular buffering of Sr2+ was less efficient than Ca2+, leading to broader activation of release sites.
Conclusions:
- Sr2+-mediated asynchronous release results from less efficient intraterminal buffering compared to Ca2+.
- This difference in buffering allows Sr2+ to activate release over a wider area near presynaptic channels.
- The findings explain the role of endogenous buffers and lack of specific facilitation between Ca2+- and Sr2+-mediated release.