Abstract
THE identification of a specific opiate receptor in mammalian brain1, and also of an endogenous morphine-like factor, enkephalin, which possesses potent opiate agonist activity peripherally2, raises the question of the possible physiological significance of this substance in the central nervous system. There is evidence from a number of studies suggesting that the brainstem is an important site for antinociceptive action3–5. In previous studies8, morphine applied iontophoretically to single neurones in the rat brainstem, has been found to cause either an increase or a decrease in firing rate, but only the depressant response showed stereospecificity and could be blocked by the specific opiate antagonist, naloxone7,8. Similar findings on cortical neurones have been reported9. We have therefore investigated the effects of iontophoretically applied methionine-enkephalin (met-enkephalin), the more potent peripherally of the two pentapeptides, on the activity of single neurones in the rat brain stem and compared these effects with those of morphine, and also of another narcotic analgesic, etorphine, which is considerably more potent. Since naloxone has been shown to block peripheral effects of enkephalin10, we have examined its effects on the neuronal responses to met-enkephalin, morphine and etorphine. Our findings support the concept of a physiological role for endogenous enkephalin in the central nervous system.
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BRADLEY, P., BRIGGS, I., GAYTON, R. et al. Effects of microiontophoretically applied methionine-enkephalin on single neurones in rat brainstem. Nature 261, 425–426 (1976). https://doi.org/10.1038/261425a0
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DOI: https://doi.org/10.1038/261425a0
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