Action of morphine on rat cortical neurons intracellularly recorded in vivo: evidence for an excitatory postsynaptic effect which is naloxone insensitive.
The action of morphine, applied either iontophoretically (40-200 nA balanced current) or systemically (5-10 mg/kg, intraperitoneally) to rat cortical neurons, was investigated in vivo, using intracellular electrodes. Morphine increased the apparent input resistance and increased the number of both spontaneous and evoked action potentials. Several cells, which normally generated single spikes, generated bursting potentials; neurons with bursting activity increased their activity. Naloxone, iontophoretically or systemically applied, did not reverse or prevent the morphine-induced excitation. The iontophoretic administration of cadmium suggested that the effects of morphine were due, at least in part, to a postsynaptic site of action. It is suggested that the increase of cellular excitability induced by morphine could contribute to its production of seizures in cortex.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002104:Cadmium / Q000494:pharmacology; D002540:Cerebral Cortex / Q000187:drug effects / Q000502:physiology*; D004558:Electric Stimulation; D008297:Male; D009020:Morphine / Q000494:pharmacology*; D009270:Naloxone / Q000494:pharmacology*; D009474:Neurons / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D013569:Synapses / Q000187:drug effects / Q000502:physiology*
D002104:Cadmium; D009270:Naloxone; D009020:Morphine