The sensation of pain cannot accurately be described as "located" at the point of an injury, or, for that matter, in any one place in the nerves or brain. Rather, pain signals-and pain relief-are delivered through a highly (5) complex interacting circuitry.
When a cell is injured, a rush of prostaglandin's sensitizes nerve endings at the injury. Prostaglandins are chemicals produced in and released from virtually all mammalian cells when they are injured: these are the only (10) pain signals that do not originate in the nervous system. Aspirin and other similar drugs (such as indomethacin and ibuprofen) keep prostaglandins from being made by inter- fering with an enzyme known as prostaglandin synthetase, or cyclooxygenase. The drugs' effectiveness against pain is (15) proportional to their success in blocking this enzyme at the site of injury.
From nerve endings at the injury, pain signais move to nerves feeding into the spinal cord. The long, tubular membranes of nerve cells carry electrical impulses. When (20) electrical impulses get to the spinal cord, a pain-signaling chemical known as substance P is released there.
Substance P then excites nearby neurons to send impulses to the brain. Local anesthetics such as novocaine and xylocaine work by blocking the electrical transmission (25)along nerves in a particular area. They inhibit the flow of sodium ions through the membranes, making the nerves electrically quiescent; thus no pain signals are sent to the spinal cord or to the brain.
1. The passage is primarily concerned with
(A) analyzing ways that enzymes and other chemicals influence how the body feels pain
(B) describing the presence of endorphins in the brain and discussing ways the body blocks pain within the brain itself.
(C) describing how pain signals are conveyed in the body and discussing ways in which the pain signals can be blocked