Journal
JOURNAL OF NEUROCHEMISTRY
Volume 76, Issue 1, Pages 258-268Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1046/j.1471-4159.2001.00019.x
Keywords
alpha-conotoxins; nAChR beta 2 null mutation; synaptosomes
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Funding
- NIDA NIH HHS [DA-03194, DA-12242] Funding Source: Medline
- NIMH NIH HHS [MH53631] Funding Source: Medline
- NATIONAL INSTITUTE OF MENTAL HEALTH [R29MH053631, R01MH053631] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [R01DA012242, R01DA003194] Funding Source: NIH RePORTER
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Acetylcholine release stimulated by nicotinic agonists was measured as radioactivity released from perfused synaptosomes prepared from mouse interpeduncular nucleus (IPN) that had been loaded with [H-3]choline. Agonist-stimulated release was dependent upon external calcium and over 90% of released radioactivity was acetylcholine. The release process was characterized by dose response curves for 13 agonists and inhibition curves for six antagonists. alpha -Conotoxin MII did not inhibit this release, while alpha -conotoxin AulB inhibited 50% of agonist-stimulated release. Comparison of this process with [H-3]dopamine release from mouse striatal synaptosomes indicated that different forms of nicotinic acetylcholine receptors (nAChRs) may mediate these processes. This was confirmed by assays using mice homozygous for the beta2 subunit null mutation. The deletion of the beta2 subunit had no effect on agonist-stimulated acetylcholine release, but abolished agonist-stimulated release of dopamine from striatal synaptosomes. Mice heterozygous for the beta2 subunit null mutation showed decreased dopamine release evoked by L-nicotine with no apparent change in EC50 value, as well as similar decreases in both transient and persistent phases of release with no changes in desensitization rates.
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