The Contribution of cocoa additive to cigarette smoking addiction

RIVM report 650270002 Page 147 of 207
Phenylethylamine
induced an increase in acetylcholine release in the striatum at 15-45 min. The
extracellular acetylcholine level in the striatum was significantly decreased by
local application of phenylethylamine (10 and 100 µM) in the striatum via a
microdialysis probe. It was concluded that systemic administration of
phenylethylamine increases acetylcholine release, whereas locally applied
phenylethylamine decreases striatal acetylcholine release in freely moving rats.
The dopaminergic system, through the dopamine D-2 receptor, seems to be
involved in the locally applied phenylethylamine-induced decrease in
acetylcholine in the striatum (18).
The cerebrovascular actions of phenylethylamine, an amine that has been
implicated in the pathogenesis of migraine, were investigated in 16 anesthetized
baboons. The influence of monoaminergic blocking agents and of a specific
inhibitor of monoamine oxidase upon the cerebral circulatory and metabolic
actions of phenylethylamine were examined. The reductions in cerebral blood
flow (28 percent) and cerebral oxygen consumption (31 percent) that accompany
the intracarotid administration of phenylethylamine (24.2 µg/kg body weight/min)
were unaffected by the prior administration of either phenoxybenzamine (1.5
mg/kg bodyweight,iv) or pimozide (0.5 mg/kg body weight, iv). The
administration of phenoxybenzamine and pimozide per se did not significantly
disturb cerebral blood flow or oxygen consumption. The ability of migraine
patients to oxidatively deaminate phenylethylamine is reduced at the time of their
attacks. The administration of the monoamine oxidase type B inhibitor, deprenyl
(1 mg/kg body weight, iv), did not effect significant changes in cerebral blood
flow or cerebral oxygen consumption. However, following deprenyl, the
administration of phenylethylamine (4.8 µg/kg body weight/min), a concentration
which was without effect in normal animals, significantly reduced cerebral blood
flow (19).
The effects of phenylethylamine (6.25, 12.5, and 25.0 mg/kg body weight, i.p.) on
spontaneous motor activity were examined in rats before (novel situation) and
after they had experience of the test environment (familiar situation), in an
undrugged state. In a novel cage, 12.5 mg/kg phenylethylamine stimulated rearing
and locomotion. A dose of 25.0 mg/kg phenylethylamine also increased rearing
and produced stereotyped head movements, but did not increase locomotion, in a
novel environment. In a familiar cage, both 12.5 and 25.0 mg/kg
phenylethylamine stimulated locomotion and sniffing, whereas rearing was
unaffected by phenylethylamine treatment under these conditions. These data
provide a striking instance of a qualitative change in the behavioural response to a
psychostimulant compound which is associated with the relative familiarity of the
animal with the test environment. In addition, the results show that
phenylethylamine induces stereotypy at high doses and increases locomotor
activity at moderate doses, which is a further illustration of the similarity in the
unconditioned behavioural effects of phenylethylamine and amphetamine (20).
autonomic system: The autonomic effects of phenylethylamine may be largely
mediated by catecholamine release from sympathetic nerve endings. The central
effects appear to be mediated in part by release of catecholamines and serotonin
and in part by direct stimulation of specific receptors. The peripheral
sympathomimetic effects of phenylethylamine is prevented by catecholamine