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Raiteri M, Bonanno G, Marchi M, Maura G. 
“Is There a Functional Linkage Between Neurotransmitter Uptake Mechanisms and Presynaptic Receptors?”. 
The Journal of Pharmacology and Experimental Therapies. 1984 Jul;23(3):671-677.
The possibility of interaction between neurotransmitter uptake mechanisms and presynaptic receptors reglating transmitter release was investigated using rat brain synaptosomes in superfusion. Various conditions were considered including: 1) absence of substrate for the uptake with uptake potentiality operative; 2) absence of substrate and presence of uptake inhibitors; and 3) uptake activated by added substrte, with or without uptake inhibitors. The release of [3H]-5-hydroxytryptamine ([3H]-5-HT) evoked by 15 mM Kcl from cerebral cortex synaptosomes was inhibited by lysergic acid diethylamide. The 5-HT uptake inhibitors citalopram and chlorimipramine did not affect the inhibitory action of lysergic acid diethylamide. Clonidine decreased both the K+ evoked release of [3H]norepinephrine and that of [3H]-5-HT in cortical synaptosomes through the activation of presynaptic alpha-2 adrenoceptors. In superfusion conditions, the action of clonidine on [3H]norepinephrine release was not antagnoized by the norepinephrine uptake inhibtors desipramine or cocaine; similarly, the inhibition of [3H]-5-HT release was unaffecte when 5-HT uptake was blocked. The K+ -evoked release of [3H]dopamine from striatal nerve terminals was ptentiated by acetylcholine (Ach) through the activation of muscarinic presynaptic receptors. The action of Ach was not modified by the presence of nomifensine, a dopamine uptake inhibitor. Finally, in superfused cortical synaptosomes, the block of the high-affinity uptake of choline by hemicholinium-3 had no effect on the muscarinic autoreceptor-mediated inhibition of [3H]ACh release by Ach. Altogether the present results do not support the previously proposed idea that in nerve terminals a functional coupling may exist between uptake mechanisms and presynaptic receptors.
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