Abstract
S-Adenosyl-L-homocysteine (SAH, 2–100 μM) greatly inhibited protein carboxymethylation (PCM) in rat striatal synaptosomes, but did not alter the ability of apomorphine and other DA agonists to inhibit DA synthesis. SAH (10 μM) also did not significantly alter the ability of either 0.5 or 1.0 μM apomorphine to inhibit DA release from superfused rat striatal tissue slices, but it did antagonize the response to 5.0 μM apomorphine. The former two concentrations of apomorphine predominantly affected only DA release, whereas the latter concentration suppressed both DA and acetylcholine release. These findings are discussed with regard to the possible relationship between DA autoreceptor functioning and PCM activity.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
