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filingDate 1996-12-06-04:00^^<http://www.w3.org/2001/XMLSchema#date>
grantDate 1998-07-14-04:00^^<http://www.w3.org/2001/XMLSchema#date>
inventor http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_782e37be9f1f3d96314a87bef8eb58e4
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_64065a8a7247613368326c2a8b4c73cd
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publicationDate 1998-07-14-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber US-5780433-A
titleOfInvention Use of α-conotoxin MII to treat disorders resulting from nicotine stimulated dopamine release
abstract Neuronal nicotinic acetylcholine receptors (nAChRs) are believed to mediate nicotine addiction. In addition, stimulation of nAChRs modulates release of neurotransmitters including dopamine, norepinephrine and serotonin. Thus, pharmacological manipulation of nicotinic receptors has implications for a wide variety of disorders including psychotic, mood, movement and cognitive. For most nAChRs, there are no subtype selective ligands. However, alpha -conotoxin MII, a small peptide from the carnivorous marine snail Conus magus, was recently isolated. This peptide has been shown to be a specific antagonist for alpha 3 beta 2 nicotinic receptors. The peptide potently blocks part, but not all, of nicotine-stimulated dopamine release from rat brain striatal synaptosomes. In contrast it has no effect on potassium stimulated dopamine release. Other alpha -conotoxins specifically target distinct neuronal nAChR subtypes. alpha -Conotoxins thus represent new lead compounds for CNS disorders.
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