Stimulation of hypothalamic arcuate nucleus inhibits locus coeruleus unit activity: evidence for endorphin mediation.
We have investigated the effect of arcuate nucleus stimulation on locus coeruleus unit activity. Extracellular LC unit activity was recorded in anesthetized cats and rats. Brief conditioning trains (25-300 microA, three shocks, 100 Hz) delivered to the arcuate nucleus produced profound inhibition (average 1000 msec, n = 30) of spontaneous coerulear cell discharges. Intravenously administered naloxone (2.5-5.0 mg/kg) or iontophoretically applied naloxone eliminated arcuate-elicited inhibition. Additionally, naloxone often increased spontaneous cell activity. In contrast to naloxone, systemically administered morphine inhibited spontaneous LC unit activity in a dose-related fashion and augmented the hypothalamic-derived inhibition. Naloxone, 5 mg/,g, reversed morphine activity to beyond predrug levels. To characterized the stereospecificity of the response, dextrorphan was administered. This inactive enantiomer failed to mimic morphine actions on LC cells. The results suggest that LC may be influenced by the beta-endorphine system originating from the arcuate nucleus.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D003917:Dextrorphan / Q000494:pharmacology; D004558:Electric Stimulation; D004723:Endorphins / Q000502:physiology*; D007031:Hypothalamus / Q000187:drug effects / Q000502:physiology*; D008125:Locus Coeruleus / Q000502:physiology*; D008297:Male; D009020:Morphine / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D004723:Endorphins; D003917:Dextrorphan; D009270:Naloxone; D009020:Morphine