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Presynaptic nicotinic receptors modulating dopamine release in the rat striatum
S Wonnacott1, S Kaiser, A Mogg
1Department of Biology and Biochemistry, University of Bath, 4 West, Bath, UK. s.wonnacott@bath.ac.uk
European Journal of Pharmacology
|April 20, 2000
Summary
Presynaptic nicotinic acetylcholine receptors modulate dopamine release in the striatum. Beta2-containing receptors on dopamine terminals directly mediate release, while others may indirectly enhance it via glutamate.
Area of Science:
- Neuroscience
- Neuropharmacology
- Cellular Biology
Background:
- Presynaptic nicotinic acetylcholine receptors (nAChRs) are known to modulate striatal dopamine release.
- Studies using synaptosomes and brain slices have provided evidence for this modulation.
Purpose of the Study:
- To compare dopamine release evoked by nicotinic receptor agonists in striatal synaptosome and slice preparations.
- To investigate the localization of specific nAChR subtypes in the striatum.
Main Methods:
- Comparison of [3H]dopamine release from striatal synaptosomes and slices using nicotinic receptor agonists (-)-nicotine and (+/-)-anatoxin-a.
- Assessment of mecamylamine-sensitive release and the effect of glutamate receptor antagonists.
- Immunogold electron microscopy using a beta2-specific monoclonal antibody to localize nAChR subtypes.
Main Results:
- Higher agonist concentrations resulted in greater mecamylamine-sensitive [3H]dopamine release from slices compared to synaptosomes.
- This increased release in slices was abolished by glutamate receptor antagonists.
- Immunogold electron microscopy showed beta2-subunit-containing nAChRs localized to symmetric (dopaminergic) synapses in the striatum.
Conclusions:
- Dopamine release is mediated by beta2-containing nAChRs located on dopamine terminals.
- Non-beta2-containing nAChRs may indirectly enhance dopamine release by stimulating glutamate release from adjacent terminals.