Regulating the supply of dopamine, a neurotransmitter, could be the first step towards a therapeutic cure for cocaine addiction, schizophrenia and Parkinson's disease
COCAINE is the single-most abused drug
in the us. Researchers from the
University of North Carolina, Chapel
Hill and the Howard Hughes Medical
Institute of the Duke University, both in
the us, have taken the first step towards,
what they claim, a therapeutic cure for
addiction of cocaine and other drugs.
Their study on a group of genetically
manipulated mice is also yielding
fresh ideas for treating disorders like
Parkinson's disease and schizophrenia.
Symptoms like addictive behaviour essentially have to do with a brain chemical - cloparnme. Moreover, too much doparnme in certain parts of the brain makes the patient schizophrenic and too little can lead to the tremors and rigidity associated with Parkinson's disease.
Doparnine, essentially a neurotransmitter, is released by one nerve cell to send a signal to another. It activates the receptor site in the synapse, the joint of the nerve cells. Normally the cell that releases cloparnine reclaims it within a fraction of a second and the signal shuts off. The reclaiming is triggered off by a certain class of protein called the cloparnine transporter, a molecule in the synapse which helps the dopamine back into the cell it was released from.
The researchers tinkered with this faculty of the nerve cells in the mice. They knocked out the gene responsible for activating the doparnine transporter in the mice and the creatures, aptly, were dubbed as 'knockouts'. Once doparnine was released in the brains of the knockouts, the signal persisred for more than 100 seconds, an unusually long time by neurosignal transmission time standards.
The lasting signal, transmitted and amplified by a million synapses ends up making the mouse very 'hyper'- The animals run around for hours together, fad to eat enough to maintain i7healthy physique and often drop dead from exhaustion. Researchers specialising in psych4harmacology (like Marc Caron from Duke University) immediately rec6gnised that the frenetic state was comparable to a person high on cocaine and amphetamines.
Action of cocaine is to block the dopatmirle transmitter and the resulting long-lasting euphoria is a fallout of the excess buildup of dopamine and not a direct effect of the drug. With period intakes of cocaine the nervous system also gets used to periodic buildups of doparnine and this is the first step towards having an addiction The theory was confirmed by the fact that the mice had no effect whatsoever of cocaine, however high the dosage might be. With no doparturre transporter in them, the drug had no target to work on and no means of raising the cloparnme level in the synapses.
A promising denouement of the study is the fact that the mice were not affected by amphetamine too. Amphetamine, another widely used drug, is also known to have similar psychosomatic effects. Alan Leshner, director of the National Institute on Drug Abuse, was understandably excited by the results - hailing it as "a major advance" in the study of addictions. "The biggest single need in this country.(us) ts for a cocaine medication, we have nothing other than behavioural treatments", Leshncr said. Findings of the study support the idea that the drugs that block cocaine at the transpoLter without affecting dopamine levels could reduce addicts' cravings for the dope.
,The study also gave rise to a new idea to treat Parkinson's disease. Although the mice act very 'hyper', Caron measured the dopamine contents in their brains as 'quite low' - about the same as that in a Parkinson's patient. In patients with Parkinson's disease, the idea is to prolong the effect of what little dopamurc they already have instead of trying to replenish it.
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