Morphine and naloxone effects on olfactory evoked electrographic activity in the amygdala.
This research tested morphine and naloxone effects on evoked EEG and unit activity in 3 opiate-relevant brain areas in response to electrical stimulation of the olfactory bulb in acute, unanesthesized rat preparations. Stimulation evoked clear EEG responses in the amygdala (Amyg) and sometimes in the other areas (caudate and central grey); morphine (15 mg/kg) depressed the Amyg response in some rats, but enhanced it in others, and naloxone usually reversed both kinds of effect. Stimulation caused excitatory unit impulse reponses in the Amyg, and morphine unexpectedly increased the magnitude of the stimulus-evoked excitation; naloxone reversed this enhancement. In control rats, naloxone often decreased the Amyg evoked response. Stimulus-evoked increases in unit activity in the caudate and central grey, when they did occur, were depressed by morphine, but naxoxone had no consistent reversing effect. Both the EEG and unit data indicate that morphine excites, or disinhibits, certain neurons associated with the olfactory-Amyg pathway. There was also some evidence that this pathway contains endorphinergic elements.
D000679:Amygdala / Q000033:anatomy & histology / Q000187:drug effects* / Q000502:physiology; D000818:Animals; D002421:Caudate Nucleus / Q000187:drug effects; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects; D005260:Female; D008297:Male; D009020:Morphine / Q000494:pharmacology*; D009270:Naloxone / Q000494:pharmacology*; D009830:Olfactory Bulb / Q000502:physiology*; D051381:Rats; D013997:Time Factors
D009270:Naloxone; D009020:Morphine