Abstract
A nociceptive stimulus (e.g., foot pinch) produced a significant increase in firing in cells in the nucleus reticularis gigantocellularis (NRGC) and surrounding areas of the rat brain. Substance P (SP), a putative nociceptive neurotransmitter, infrequently produced an increase in spontaneous neuronal firing when administered microiontophoretically to these areas. These data indicate that the NRGC is an area involved in nociception. However, SP does not appear to be the primary nociceptive neurotransmitter or neuromodulator in the NRGC because SP did not mimic or enhance the response to the nociceptive stimulus. Morphine (MS) and methionine-enkephalin (ENK), administered microiontophoretically, rarely had any effect on spontaneous neuronal firing or rarely modified the increase in neuronal firing evoked by the nociceptive stimulus. For this reason, the NRGC is apparently not an area where MS and ENK act directly to produce analgesia.
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