By Janet T. Spence
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Excitatory connection; מ, inhibitory connection. Note: There is also dynamic modulation of the release of neurotransmitter from pain fibers arriving in the spinal cord from the body. Although not illustrated in the figure, pain inhibitory systems can inhibit release of neurotransmitter from these sensory fibers, and pain facilitatory systems can exaggerate the release of neurotransmitter from these sensory fibers. 32 WATKINS Ⅲ MAIER of the pain message being relayed to the brain (Sandkuhler 1996, Watkins & Maier 1997, Yaksh 1997, Zimmermann & Herdegen 1996).
What these circuits have in common is that, in the end, they send axons from sites in the brain down to the spinal cord, where pain signals are inhibited (Figure 1). These circuits can also be activated directly, by systemic administration of drugs, such as morphine, or by implantation of either fine wires or tubes into discrete sites along these pathways that allow their activation by electrical stimulation or drug microinjection, respectively (Richardson 1995, Sandkuhler 1996, Yaksh 1997). Animal studies of analgesia produced by such direct activation of these pathways led to the development of many analgesic drugs and to the use of brain stimulators and epidural drug injections for control of pain in humans.
From this point, the neurocircuitry for each sickness response likely diverges as axons from the nucleus tractus solitarius project to the multiple brain regions mediating various sickness outcomes. From lesion studies it is known that sickness-induced hyperalgesia involves, at least, the nucleus tractus solitarius and the nucleus raphe magnus (see Figure 2), with the latter structure sending its axons down to the spinal cord dorsal horns where exaggerated pain responses are created (Watkins & Maier 1999a).