Science: Under the Microscope: Cocaine running around the brain

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The Independent Culture
At Sydney airport a magazine caught my eye. The cover promised a "vital guide" to "Drugs: what every parent should know." I bought the issue and learnt that the easy to read but comprehensive summary of drugs of abuse was inspired by a tragedy reminiscent of that of Leah Betts.

A 15-year-old Sydney teenager, Anna Wood, had taken an ecstasy tablet at a party. Within hours she was vomiting and disorientated. The next day she was in a coma. Two days later she died. Anna's mother had appealed to the Federal Government to make more information on drugs available: The Australian Women's Weekly had taken up the challenge.

The eight-page booklet was superb: it dispassionately described the appearance, effects, and dangers of marijuana, benzodiazepine tranquillisers, heroin, cocaine, ecstasy, speed, and LSD. Then I thought, why stop there? Why not explain how the drugs work within the brain?

The brain is made up of cells. Ninety per cent conduct operations that are still not fully known: in the main, however, they act as house-keepers, ensuring a benign and nurturing environment for the remaining 10 per cent of their company to carry out one particular task. This specialised minority of brain cells number an awesome 100 billion in the human brain: they have the capacity for sending very fast signals to each other. The generation of such signals via neurons is the building block of all that the brain can do.

Think of the neuron as a cartoon dynamite ball with a long fuse attached. Imagine how it would look if the fuse was ignited, but the film played in reverse: first you would see and hear the explosion in the main part of the device, then the flame would creep further and further away, down the fuse to the end. In a neuron, the explosion is an electrical signal lasting a thousandth of a second, that races down the fuse of the neuron, at up to 250 miles an hour.

But thereafter brain electricity on its own can do nothing, because there is a gap between the ends of the extensions of the sending and receiving neurons. Nature's trick is to make the electrical pulse trigger the release of a chemical messenger, a "transmitter", that crosses the gap between the two neurons. The electrical signal is converted into a chemical one, and here drugs leave their mark. Some - amphetamines, ecstasy, cocaine - can cause too much transmitter to be released, and not enough to be removed. Others, like nicotine or heroin, artificially stimulate chemical target sites on the receiving neurons, which enable the next cell along to generate its own electrical signal. If this target is bombarded too often, it will become less sensitive to adjust to the incessant stimulation - like eventually ignoring someone shouting all the time. Consequently, chemicals have to shout still louder - more is needed to have the same original effect. This is the basis of addiction.

Just because they work at similar stages in the neuronal process of communication, does not mean to say that nicotine and heroin are the same: far from it. Rather, most drugs will interfere with only one type of transmitter, of which there are at least some 50 or 60 currently in your brain. This is why different drugs have different, often quite opposite effects. Because each transmitter is at work in different regions of the brain, it has a multiplicity of tasks: hence any interference aimed at just one of those tasks, will also entail interference with the others: side effects.

We can describe how drugs disrupt the nuts and bolts of the brain, but we cannot say how those neuronal nuts and bolts are translated into memory, personality and pleasure. If people tempted to marinate their minds in chemicals, learnt more about how much - and how little - we understand drug action in the brain, they might think twice.

! Susan Greenfield is a neuroscientist at the University of Oxford, and Gresham Professor of Physics, London.

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