Abstract

This may sound like a dry topic, but it's not. T h e concept of presynaptic inhibition of primary afferents is appealing to theoreticians. primarily for clinical reasons. There is an overwhelming amount of evidence that inhibition of pain perception can and does occur in the nervous system. Clinical observations have documented many instances, such as battle injuries and sports injuries, where perception of an appropriate painful stimulus is effectively suppressed, sometimes for long periods of time. The dramatic selective effect of opiates, which mimic enkephalin neurotransmitters, on pain perception is further clinical evidence for specific neural mechanisms to inhibit pain. Various animal studies have documented that a variety of behavioral, pharmacologic, and CNS stimulation manipulations can produce profound and specific analgesic effects. Neuronal recording studies have documented that nociception (responsiveness to presumably painful stimulation) can be suppressed in secondary neurons in the dorsal horn of the spinal cord--the first relay after primary afferents--by many of the manipulatfons mentioned above. There are several ways that neural circuitry could be arranged to cause this inhibition. Two dominant themes in proposals for such circuitry are inhibitory effects on the spinal cord neurons themselves (postsynaptic inhibition), and inhibitory effects on primary afferents which prevent therri from activating secondary

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