Mu and kappa opioid modulation of olfactory bulb evoked potentials.
Modulatory influences of the mu opioid agonist morphine and the kappa opioid agonist U-50, 488H on field-evoked potentials from the main olfactory bulb (MOB) in response to stimulation of the olfactory nerve were studied. Topically administered morphine upon the MOB dorsal surface produced a noloxone-sensitive depression of the late component of the response without modifying the early one, while topical administration of U-50, 488H suppressed both the early and the late components. Naloxone did not antagonize U-50, 488 effects. Results indicate that mu and kappa opioid agonists can interfere with sensory transmission at the level of second-order neurons of the olfactory pathway, the mitral and/or tufted cells.
Pérez
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Laboratory of Neurophysiology and Biophysics, University of Chile, Santiago.
Hernández
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Inostroza
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D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; D000818:Animals; D009020:Morphine / Q000494:pharmacology*; D009830:Olfactory Bulb / Q000187:drug effects / Q000502:physiology*; D011759:Pyrrolidines / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains; D011957:Receptors, Opioid / Q000187:drug effects / Q000502:physiology*; D017473:Receptors, Opioid, kappa; D017450:Receptors, Opioid, mu
D011759:Pyrrolidines; D011957:Receptors, Opioid; D017473:Receptors, Opioid, kappa; D017450:Receptors, Opioid, mu; D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; D009020:Morphine