Opioid modulation of the response of preoptic neurones to stimulation of the ventral noradrenergic tract in female rats.
1. Experiments were undertaken on twenty-nine ovariectomized female rats, pretreated with oestrogen and anaesthetized with urethane, to test the hypothesis that opioid peptides regulate noradrenergic transmission in the medial preoptic area and thereby influence the neural circuitry controlling the secretion of luteinizing hormone. 2. Extracellular recordings were obtained with glass micropipettes from ninety-four neurones in the medial preoptic area. These recordings were continued whilst both the ventral noradrenergic tract, the noradrenergic projection to the medial preoptic area, and orthodromic pathways originating in the arcuate nucleus, the main source for endogenous opioid peptides in the hypothalamus, were stimulated electrically. Forty of the ninety-four neurones responded to stimulation at one or both of the test sites. 3. Electrical stimulation of the ventral noradrenergic tract excited fifteen neurones (greater than 30% change in number of action potentials recorded during the 'response time period') and inhibited a further ten cells. When the nucleus arcuatus was stimulated electrically thirteen cells were inhibited and twelve neurones showed an excitatory response. 4. The opioid antagonist naloxone (80 mM) and/or morphine (50 mM) were ejected into the immediate vicinity of eighty-six of the recorded cells by passage of balanced currents (range 15-80 nA) through a multi-barrelled electrode glued to the recording electrode. The tip of the drug-containing electrode was about 15-25 microns behind the tip of the recording electrode. 5. The ionophoretic application of naloxone, during electrical stimulation of the ventral noradrenergic tract, diminished the inhibitory response in four of ten cells and enhanced the excitatory response in nine out of fifteen neurones. By contrast, morphine diminished the excitatory response in seven of these fifteen cells tested, an effect that was prevented by the simultaneous application of naloxone. 6. Similarly, the application of naloxone during stimulation of the nucleus arcuatus reduced the inhibitory effect in eight out of thirteen cells. When four of these eight responsive neurones were exposed to morphine either the effect of naloxone was reversed or, when given alone, the inhibition was enhanced. 7. Finally, for seventeen cells categorized as non-responsive to stimulation at either site, the application of naloxone during hind brain stimulation revealed an excitatory input from the ventral noradrenergic tract in seven cases. 8 The experiments demonstrate that opioid peptides modulate the neural inputs to the medial preoptic area arising from the nucleus arcuatus and the ventral noradrenergic tract.(ABSTRACT TRUNCATED AT 400 WORDS)
AFRC Institute of Animal Physiology and Genetics Research, Babraham, Cambridge.
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Dyer
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Grossman
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001111:Arcuate Nucleus of Hypothalamus / Q000502:physiology; D004723:Endorphins / Q000502:physiology*; D005260:Female; D008526:Medulla Oblongata / Q000502:physiology; D009020:Morphine / Q000494:pharmacology; D009270:Naloxone / Q000494:pharmacology; D009434:Neural Pathways / Q000502:physiology; D009474:Neurons / Q000502:physiology*; D011301:Preoptic Area / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D004723:Endorphins; D009270:Naloxone; D005680:gamma-Aminobutyric Acid; D009020:Morphine