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Deprenyl and (-)1-phenyl-2-propylaminopentane, [(-)PPAP], act primarily as potent stimulants of action potential-transmitter release coupling in the catecholaminergic neurons.

Knoll J, Miklya I, Knoll B, Marko R, Kelemen K.

Department of Pharmacology, 
Semmelweis University of Medicine, Budapest, Hungary.
 

Life Sci 1996;58(10):817-827

ABSTRACT

The activity of the catecholaminergic neurons in the rat brain is enhanced significantly 30 min after the subcutaneous injection of very small doses of deprenyl (threshold doses: 0.01 mg/kg for noradrenergic neurons and 0.025 mg/kg for dopaminergic neurons). As a catecholaminergic activity enhancer (CAE) substance deprenyl is about ten times more potent than its parent compound, (-)methamphetamine. While the (+)methamphetamine is 3-5 times more potent than (-)methamphetammine in releasing catecholamines, the (-)methamphetamine is the more potent CAE substance. The mechanism of the CAE effect of deprenyl and (-)PPAP, a deprenyl-derived substance devoid of MAO inhibitory potency, was studied in rats by measuring: 
a) the release of catecholamines from striatum, substantia nigra, tuberculum olfactorium and locus coeruleus; 
b) the stimulation induced release of 3H-noradrenaline from the isolated brain stem; and 
c) the antagonistic effect against tetrabenazine-induced depression of learning in the shuttle box. 
The CAE effect was found to be unrelated: 
a) to the inhibition of MAO activity; 
b) to the inhibition of presynaptic catecholamine receptors; 
c) to the inhibition of the uptake of catecholamines; and 
d) to the release of catecholamines. 

 It was concluded that deprenyl and (-)PPAP act primarily as potent stimulants of action potential-transmitter release coupling in the catecholaminergic neurons of the brain.  We show that both deprenyl and (-)PPAP enhance the inward Ca2+ current in sino-auricular fibers of the frog heart. (-)PPAP was much more potent than either (+)PPAP or deprenyl in this test.

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