Neuroscience 2004 Abstract
| Presentation Number: | 956.16 |
|---|---|
| Abstract Title: | Alpha-conotoxin Bu13, a selective antagonist for nicotinic acetylcholine receptor-mediated neurotransmitter release. |
| Authors: |
Grady, S. R.*1
; McIntosh, J. M.2,3
; Laudenslager, E.1
; Collins, A. C.1
; Marks, M. J.1
1Inst Behav Genet., Univ Colorado, Boulder, CO 2UT, Campus Box 447, 80309, 3USA, Campus Box 447, 80309, |
| Primary Theme and Topics |
Synaptic Transmission and Excitability - Ligand Gated Ion Channels -- Nicotinic acetylcholine receptors |
| Session: |
956. Nicotinic Acetylcholine Receptors: Pharmacology Poster |
| Presentation Time: | Wednesday, October 27, 2004 4:00 PM-5:00 PM |
| Location: | San Diego Convention Center - Hall A-H, Board # J20 |
| Keywords: | nicotine, dopamine, striatum, nicotinic receptor |
α-Conotoxin Bu1.3 (Bu1.3) was shown to be useful in differentiating norepinephrine release mediated by β2*-nAChRs in mice from β4*-nAChRs in rats (Azam et al., SFN, 2003). Here we have investigated the selectivity of Bu1.3 in differentiating β2*-nAChR mediated dopamine (DA) release from striatal synaptosomes of wildtype and nAChR subunit null mutant mice. In addition, the β4*-nAChR mediated acetylcholine release from wildtype mouse IPN was compared. Results show that 1) though competitive, Bu1.3, like α-conotoxin MII (MII), acts as a noncompetitive inhibitor because of slow off-rate kinetics. 2) Both α4 null mutant and α4β3 double null mutant mice have MII- and Bu1.3-sensitive DA release activity and no toxin resistant activity. 3) The onset of and recovery from Bu1.3 with β2*-nAChR-mediated DA release are faster than with MII. Onset and recovery from Bu1.3 are also measurably faster in wildtype mice than in α4 null mutant or α4β3 double null mutant mice. 4) IC50 values for inhibiting DA release from wildtype, α4 null mutant and α4β3 double null mutant mice differ somewhat (0.3nM, 0.9nM and 1.3nM, respectively). 5) Onset and recovery with Bu1.3 are much slower for inhibition of β4*-nAChR mediated ACh release from IPN, and the IC50 value is significantly higher (100nM).
Supported by DA12242, DA03194, DA015663, MH53631
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.
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