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We may experience pain as a prick, tingle, sting, burn, or ache. Receptors on
the skin trigger a series of events, beginning with an electrical impulse that
travels from the skin to the spinal cord. The spinal cord acts as a sort of
relay center where the pain signal can be blocked, enhanced, or otherwise modified
before it is relayed to the brain. One area of the spinal cord in particular,
called the dorsal horn, is important in the reception of pain signals.
The most common destination in the brain for pain signals is the thalamus and
from there to the cortex, the headquarters for complex thoughts. The thalamus
also serves as the brain's storage area for images of the body and plays a key
role in relaying messages between the brain and various parts of the body. In
people who undergo an amputation, the representation of the amputated limb is
stored in the thalamus.
Pain is a complicated process that involves an intricate interplay between
a number of important chemicals found naturally in the brain and spinal cord.
In general, these chemicals, called neurotransmitters, transmit nerve
impulses from one cell to another.
There are many different neurotransmitters in the human body; some play a role
in human disease and, in the case of pain, act in various combinations to produce
painful sensations in the body. Some chemicals govern mild pain sensations;
others control intense or severe pain.
The body's chemicals act in the transmission of pain messages by stimulating
neurotransmitter receptors found on the surface of cells; each receptor
has a corresponding neurotransmitter. Receptors function much like gates or
ports and enable pain messages to pass through and on to neighboring cells.
One brain chemical of special interest to neuroscientists is glutamate.
During experiments, mice with blocked glutamate receptors show a reduction in
their responses to pain. Other important receptors in pain transmission are
opiate-like receptors. Morphine and other opioid drugs work by locking on to
these opioid receptors, switching on pain-inhibiting pathways or circuits, and
thereby blocking pain.
Another type of receptor that responds to painful stimuli is called a nociceptor.
Nociceptors are thin nerve fibers in the skin, muscle, and other body tissues,
that, when stimulated, carry pain signals to the spinal cord and brain. Normally,
nociceptors only respond to strong stimuli such as a pinch. However, when tissues
become injured or inflamed, as with a sunburn or infection, they release chemicals
that make nociceptors much more sensitive and cause them to transmit pain signals
in response to even gentle stimuli such as breeze or a caress. This condition
is called allodynia -a state in which pain is produced by innocuous stimuli.
The body's natural painkillers may yet prove to be the most promising pain
relievers, pointing to one of the most important new avenues in drug development.
The brain may signal the release of painkillers found in the spinal cord, including
serotonin, norepinephrine, and opioid-like chemicals. Many pharmaceutical companies
are working to synthesize these substances in laboratories as future medications.
Endorphins and enkephalins are other natural painkillers. Endorphins
may be responsible for the "feel good" effects experienced by many people after
rigorous exercise; they are also implicated in the pleasurable effects of smoking.
Similarly, peptides, compounds that make up proteins in the body, play
a role in pain responses. Mice bred experimentally to lack a gene for two peptides
called tachykinins-neurokinin A and substance P-have a reduced response to severe
pain. When exposed to mild pain, these mice react in the same way as mice that
carry the missing gene. But when exposed to more severe pain, the mice exhibit
a reduced pain response. This suggests that the two peptides are involved in
the production of pain sensations, especially moderate-to-severe pain. Continued
research on tachykinins, conducted with support from the NINDS, may pave the
way for drugs tailored to treat different severities of pain.
Prepared by: Office of Communications and Public Liaison
National Institute of Neurological Disorders and Stroke
National Institutes of Health
Bethesda, MD
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