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Characterization of DIDS-sensitive ATP accumulation in brain synaptic vesicles
Ran Zalk1, Varda Shoshan-Barmatz
1Department of Life Sciences, National Institute for Biotechnology, Negev and Zlotowski Center for Neuroscience, Ben Gurion University, Life Sciences Building 40, 84105 Beer Sheva, Israel.
FEBS Letters
|October 10, 2006
Summary
Adenosine triphosphate (ATP) accumulation in brain synaptic vesicles (SVs) does not follow a concentration gradient. This suggests a unique, proton-independent transport mechanism for this excitatory neurotransmitter.
Area of Science:
- Neuroscience
- Cell Biology
- Neurochemistry
Background:
- Adenosine triphosphate (ATP) functions as an excitatory neurotransmitter in both central and peripheral nervous systems.
- Understanding the mechanisms of neurotransmitter packaging into synaptic vesicles (SVs) is crucial for synaptic function.
- Previous models of neurotransmitter transport often involve proton gradients or exchange mechanisms.
Purpose of the Study:
- To investigate the mechanism of ATP accumulation in highly purified brain synaptic vesicles (SVs).
- To determine if ATP transport into SVs occurs against a concentration gradient.
- To identify factors influencing ATP transport into SVs.
Main Methods:
- Isolation of highly purified brain synaptic vesicles (SVs).
- Measurement of ATP accumulation within SVs under various experimental conditions.
- Assessment of the effects of inhibitors (DIDS, NEM) and other substances (Mg2+, nucleotides) on ATP transport.
Main Results:
- ATP accumulation in SVs was observed, but not against a concentration gradient.
- The transport mechanism appears to be independent of the proton motive force (Delta mu H(+)).
- ATP transport was inhibited by DIDS and NEM, but unaffected by Mg2+ or pre-incubation with other nucleotides.
Conclusions:
- Brain synaptic vesicles (SVs) possess a unique ATP transport system.
- This mechanism is distinct from known neurotransmitter transporters, as it does not rely on proton exchange.
- The findings suggest a novel pathway for regulating extracellular ATP levels and neurotransmission.
