Inside the Addict's Brain
have recently been worked out describing events in any brain
exposed to the most common addictive drugs: heroin, morphine,
barbiturates, tranquillisers, and alcohol (all depressants that
slow down processes in the brain and central nervous system);
and cocaine, amphetamines, nicotine, and marijuana (all stimulants
that generally excite them).
As the target
organ of addiction, brain cells react to stimuli, including
substances introduced from outside and hormones and chemicals
we make ourselves. Those reactions lead to other chemical reactions
and to changes in movement, thought, feelings, and memory. Drugs
of abuse abet, or interfere with the chemical messengers, or
neurotransmitters. The neurotransmitters that facilitate addiction
are released by the 10 billion neurones that deal with information
circulate, collect, and act at specific sites on nearby cell
surfaces called receptor proteins, each of which is shaped to
fit and receive a particular neurotransmitter and bind it the
way a lock "recognises" a key. Only after a neurotransmitter
binds can the signal it carries travel to the next cell. If
the cell is flooded with too much neurotransmitter, an elegant
"control" system is normally activated so that the
cell reabsorbs the excess for later use. This process, called
"reuptake," prevents too many chemical signals from
circulating and filling too many receptors, which can lead to
over-activity and serious mental and physical problems.
now know that some abused substances block re-absorption, leaving
too much neurotransmitter around. Others block the release of
neurotransmitters. Although many neurotransmitters and chemicals
that act like them have been identified, those most notably
linked to addiction are norepinephrine, dopamine, serotonin,
substance P and gamma-aminobutyric add (GABA).
Solomon Snyder, M.D., director of neuroscience at Johns Hopkins
and his then-graduate student Candace Pert, put a solid foundation
under the new theory of addiction by finding receptors for opium
in the brain. They accomplished this by tracking molecules of
the drug with radioactive tags to their binding sites. Derivatives
of heroin and morphine bind to those same sites. Methadone,
a weak synthetic opiate, binds less tightly; one reason it satisfies
an addict's craving is that it is addictive but does not produce
and Pert also understood that their discovery had far greater
implications. For if the brain had opiate receptors, it surely
wasn't because nature intended man to fall victim to heroin
addiction, but because the body itself must produce opiates.
The discovery in 1975 of the brain's own opiates, called endorphins
or enkephalins, demonstrated neurochemical sites of pleasure
in the brain activated naturally by human activity.
would learn that opiates keep opiate receptors constantly full,
producing the physical tolerance so characteristic of heroin
addiction. They discovered that the opiate-addicted brain also
appears to close off some receptors so that desensitisation
occurs, encouraging larger and larger doses.
that cocaine affects nerve cells in the limbic system, the most
ancient part of the brain and one closely tied to emotions.
But rather than bind to a receptor, it interrupts the process
of reuptake that terminates the action of dopamine. Cocaine
is not only a blocker of dopamine uptake but of the reuptake
of serotonin and norepinephrine as well.
All of this
leads to vast over-stimulation of nerve cells and creates intense
feelings of excitement and joy. With cocaine, dopamine spills
forth and floods our pleasure receptors. On the downside, cocaine
eventually wipes out the brain's existing supply of these neurotransmitters
temporarily, leading to a hellish withdrawal marked by severe
depression, paranoia, intense irritability and craving.
to Steven Childers, psychedelic drugs of abuse such as LSD and
"mushrooms" don't activate the ancient reward system
regulated by dopamine, serotonin, and norepinephrine. Moreover,
they appear to influence different parts of the brain involved
in higher functions than emotions and pleasure. "For people
who use these drugs, they are less an addiction than an intellectual
drive to alter mood and produce higher levels of consciousness,"
he says. "And when we look at how they act in the brain,
we can begin to understand why."
most common types of tranquillisers, barbiturates and benzodiazepines
(Valium and its cousins), also act differently in the brain.
They don't have their own receptors, but act on a "foster"
receptor, GABA, which is predominantly an inhibitory, or slow-down,
neurotransmitter. These drugs "deinhibit" and in sort
of a double-negative effect, increase inhibition, sedating the
user. "What these drugs do is hyperactivate inhibition,"
notes Childers. "Increase GABA enough and you shut down
the brain. That's what sedatives do." Alcohol also appears
to act on GABA receptors, amphetamines interrupt dopamine balance,
and nicotine stimulates the release of endorphins, at least
at high doses.
published in the Psychology Today