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Presynaptic modulation of amino acid release from synaptosomes
A D Sherman1, T S Hegwood, S Baruah
1Department of Psychiatry, College of Medicine, University of Iowa, Iowa City 52242.
Neurochemical Research
|February 1, 1992
Summary
This study shows that glutamate and GABA are released from rat brain synaptosomes. Presynaptic glutamate receptors modulate this release, impacting both spontaneous and calcium-dependent neurotransmitter release.
Area of Science:
- Neuroscience
- Neurochemistry
Background:
- Synaptosomes are crucial for studying neurotransmitter release mechanisms.
- Glutamate and GABA are key excitatory and inhibitory neurotransmitters, respectively.
Purpose of the Study:
- To investigate the spontaneous and calcium-dependent release of glutamate and GABA from rat brain synaptosomes.
- To determine the role of NMDA and AMPA receptors in modulating neurotransmitter release.
Main Methods:
- Preparation of synaptosomes from whole rat brain.
- Measurement of spontaneous and calcium-dependent glutamate and GABA release over 1-30 second intervals.
- Assessment of the effects of NMDA, AMPA, and antagonists on neurotransmitter release.
Main Results:
- Spontaneous glutamate release, but not GABA, was enhanced by NMDA or AMPA, partially dependent on calcium.
- KCl-induced calcium-dependent release was biphasic and stimulated by NMDA or AMPA in an antagonist-sensitive manner.
- These findings indicate modulation of vesicular release by presynaptic glutamate receptors.
Conclusions:
- Both glutamate and GABA are released from vesicular stores in rat synaptosomes.
- Presynaptic glutamate receptors play a significant role in modulating both spontaneous and evoked neurotransmitter release.