Interestingly, a pair of Canadian and English investigators speculated that such
pain-suppressing pathways must exit when they devised a new "gate theory of
pain" in the midsixties. Their idea was that when pain signals first reach the
nervous system they excite activity in a group of small neurons that form a kind of pain
"pool." When the total activity of these neurons reaches a certain minimal
level, a hypothetical "gate" opens up that allows the pain signals to be sent to
higher brain centers. But nearby neurons in contact with the pain cells can suppress
activity in the pain pool so that the gate stays closed. The gate-closing cells include
large neurons that are stimulated by nonpainful touching or pressing of your skin. The
gate could also be closed from above, by brain cells activating a descending pathway to
block pain.
The theory explained such everyday behavior as scratching a scab, or rubbing a appraised
ankle: the scratching and rubbing excite just those nerve cells sensitive to touch and
pressure that can suppress the pain pool cells. The scientists conjectured that
brain-based pain control system were activated when people behaved heroically -- ignoring
pain to finish a football game, or to help a more severely wounded soldier on the
battlefield.
The gate theory aroused both interest and controversy when it was first announced. Most
importantly, it stimulated research to find the conjectured pathways and mechanisms. Pain
studies got an added boost when investigators made the surprising discovery that the brain
itself produces chemicals that can control pain.
The landmark discovery of the pain-suppressing chemicals came about because scientist in
Aberdeen, Scotland, and at the John Hopkins University Hospital in Baltimore were curious
about how morphine and other opium-derived painkillers, or analgesics, work.
For some time neuroscientists had known that chemicals were important in conducting nerve
signals (small bursts of electric current) from cell to cell. In order for the signal from
one cell to reach the next in line, the first cell secretes a chemical
"neurotransmitter" from the tip of a long fiber that extends from the cell body.
The transmitter molecules cross the gap separating the two cells and attach to special
receptor sites on the neighboring cell surface. Some neurotransmitters excite the second
cell -- allowing it to generate an electrical signal. Other inhibit the second cell --
preventing it from generating a signal.
When investigators in Scotland and at Johns Hopkins injected morphine into experimental
animals, they found that the morphine molecules fitted snugly into receptors on certain
brain and spinal cord neurons. Why, the scientist wondered, should the human brain -- the
product of millions of years of evolution -- come equipped with receptors for a man-made
drug? Perhaps there were naturally occurring brain chemicals that behaved exactly like
morphine.
The Brain's Own Opiates
Both groups of scientists found not just one pain-suppressing chemical in the brain, but a
whole family of such proteins. The Aberdeen investigators called the smaller members of
the family enkephalins (meaning "in the head"). In time, the larger proteins
were isolated and called endorphins, meaning the "morphine within." The term
endorphins is now often used to describe the group as a whole.
The discovery of the endorphins lent weight to the general concept of the gate theory.
Endorphins released from brain nerve cells might inhibit spinal cord pain cells through
pathways descending from the brain to the spinal cord. Endorphins might also be activated
when you rub or scratch your itching skin or aching joints. Laboratory experiments
subsequently confirmed that painful stimulation led to the release of endorphins from
nerve cells. Some of these chemicals then turned up in cerebrospinal fluid, the liquid
that circulates in the spinal cord and brain. Laced with endorphins, the fluid could bring
a soothing balm to quiet nerve cells.
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