Tetrodotoxin-sensitivity of nicotine-evoked dopamine release from rat striatum
Section snippets
Synaptosomes and slices
Male Sprague–Dawley rats (240–280 g, University of Bath breeding colony) were killed by cervical dislocation, decapitated and brain striata rapidly dissected for preparing synaptosomes or slices. P2 synaptosome fractions were prepared as described previously (Soliakov et al., 1995). Percoll gradient purified synaptosomes (fraction 4) were prepared according to the procedure of Dunkley et al. (1988)as previously described by Soliakov and Wonnacott (1996). Synaptosomes were loaded with [3
Results
The first experiments compared the TTX sensitivity of nicotine-evoked [3H]dopamine release from crude P2 synaptosomes and from a purer preparation, isolated on Percoll gradients (Fig. 1(A, B), respectively). In both cases 10 μM nicotine (a concentration that is just maximally effective in striatal synaptosome preparations (Whiteaker et al., 1995)) evoked the release of [3H]dopamine, and this was inhibited by 20 μM mecamylamine, to 23±2% (n=3) of control for P2 synaptosomes and 29±8% (n=4) of
Discussion
The object of this study was to characterise the TTX-sensitivity of nicotine-stimulated dopamine release from rat striatum in superfused synaptosomes, superfused slices and by in vivo microdialysis.
Figures 1 and 2 show that TTX can inhibit nicotine-evoked dopamine release in all three experimental preparations, but to varying degrees. This is unlikely to reflect a direct interaction of TTX with the nAChR because (i) nicotine or anatoxin-a-evoked and veratridine-evoked responses are similarly
Acknowledgements
This study was supported by grants from The Wellcome Trust (038960, to P.H.R. and S.W.) and BBSRC (to S.W.).
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