Drugs online research references
Rev Neurol (Paris). 1970 Feb;122(2):141-2.
[Three cases of action myoclonus during treatment with imipramine and amitriptyline]
[Article in French]
Darcourt G, Fadeuilhe A, Lavagna J, Cazac A.
PMID: 5517898
Act Nerv Super (Praha). 1978 Dec;20(4):255-6.
The mechanism of effect of neuropharmacological drugs. V. (Effect of amitriptyline and physostigmine on free fatty acids in brain).
Sklenovsky A, Chmela Z.
PMID: 735722
Br J Pharmacol. 1980 Jun;69(2):215-25.
The relationship between nerve terminal adenosine triphosphatases and neurotransmitter release: as determined by the use of antidepressant and other CNS-active drugs.
Gilbert JC, Wyllie MG.
1 The role of adenosine triphosphatases (ATPases) in neurotransmitter release was studied using nerve terminals (synaptosomes) prepared from rat cerebral cortex as a model. 2 Amitriptyline, nortriptyline, protriptyline, desipramine and imipramine were found to inhibit ATPases at concentrations of 10(-5) M and above. The drugs inhibited both the basal and electrically evoked release of acetylcholine (ACh) and noradrenaline (NA) at concentrations of 10(-4) M and above. 3 At low concentrations of antidepressants (10(-8) and 10(-7) M) release of NA was enhanced but there was no effect on ACh release. 4 Other drugs which inhibit Na+, K+-ATPase increase basal NA release as did drugs which inhibited vesicular MG2+-ATPase. 5 A model is proposed suggesting that transmitter release/re-uptake depends on (1) active Na+, K+-ATPase at the presynaptic membrane and (2) an active synaptic vesicular MG2+-ATPase.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6108138&dopt=Abstract
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