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TIAFT BULLETIN VOLUME 41, 2011. No 1
enzyme, which means it is orally active and also more easily
crosses the blood-brain barrier.
The chemical structure of amphetamine resembles the
biogenic amines dopamine, adrenaline and norepinephrine
(noradrenaline) that transmit information between nerve
cells. This gives a clue to the way amphetamine acts in the
brain, namely as a false transmitter amine and also seems
to functioning as a re-uptake inhibitor. When amphetamine
enters a synapse it forces dopamine and noradrenaline to
be released from nerve endings into the synaptic cleft thus
facilitating binding to receptors on postsynaptic neurons.
Their ability to stimulate body functions controlled by the
sympathetic nervous system meant that amphetamine
and its analogues were referred to as sympathomimetic
amines, a term coined by the British pharmacologist and
Nobel Laureate Sir Henry Dale (1875-1968).
Central stimulants entered the spotlight in the 1990s along
with the rise in popularity of designer drugs by adolescents
belonging to the rave culture. Young people took an
ecstasy (MDMA) tablet to give them energy and to
heighten their sexual arousal and to keep awake during
all-night rave parties and dance sessions. Ecstasy combines
both stimulant (amphetamine-like) and hallucinogenic
(mescaline-like) properties by acting on receptors for both
dopamine and serotonin.
History shows that MDMA was first synthesized by the
German pharmaceutical company Merck (Darmstadt)
in 1912 in connection with research aimed at developing
drugs to prevent blood clotting. The date of the first human
studies with MDMA is not known, although its stimulant
properties became well known through the writings of
Alexander Shulgin (born 1925) as described in his book
PIHKAL. The popularity of MDMA as a recreational drug
attracted attention from government agencies after a
number of overdose deaths were reported. The lack of
any therapeutic uses of MDMA led to its classification as a
scheduled substance (class I).
There is a current trend among some teenagers to obtain
central stimulant “designer drugs” over the Internet the socalled
“legal highs”. These Internet drugs are structurally
related to amphetamine or methamphetamine and work
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by interacting with dopamine or serotonin neurotransmission.
Examples include p-methoxyamphetamine (PMA),
p-methoxymethamphetamine, 4-methylthioamphetmaine
(MTA), methedrone (4-methoxy-methcathinone),
N-benzylpiperazine (BZP or A2) and mephedrone
(4-methylmethcathinone). Many have become listed as
scheduled substances in efforts to restrict their import and
sales, but as one compound is banned another appears to
take its place. It is seemingly a simple task for clandestine
laboratories and their chemists to make a small minor
structural modification and obtained a compound that is
sufficiently different that it is not covered by the ban.
Further reading
Iversen L. Speed, Ecstasy, Ritalin - the science of
amphetamines. Oxford, Oxford University Press, 2006.
Rasmussen N. On speed: The many lives of amphetamines.
New York, New York University Press, 2008.
Rasmussen N. Making the first anti-depressant:
Amphetamine in American Medicine. J Hist Med Allied Sci
61;288-323, 2006.
Freudenmann RW, Öxler F, Bernschneider-Reif S. The origin
of MDMA (ecstasy) revisited: the true story reconstructed
from the original documents. Addiction 101:1241-1245,
2006.
Cruickshank CC, Dyer KR. A review of the clinical
pharmacology of methamphetamine. Addiction 104:1085-
1099, 2009.
Kalant H. The pharmacology and toxicology of “ecstasy”
(MDMA) and related drugs. CMAJ 165:917-928, 2001.
Benzenhöfer U, Passie T. Rediscovering MDMA (ecstasy):
the role of the American chemist Alexander T. Shulgin.
Addiction 105:1355-1361, 2010.
Stix G. Turbocharging the brain. Sci Am Oct 28-35, 2009.