Nicotinic control of tuberoinfundibular dopaminergic neuron activity and prolactin secretion: diurnal rhythm and involvement of endogenous opioidergic system.
The possible involvement of cholinergic and opioidergic neurons in the control of diurnal changes of tuberoinfundibular dopaminergic (TIDA) neuronal activity was reported. Adult Sprague-Dawley rats ovariectomized and treated with estrogen were used. All drugs were administered centrally through preimplanted intracerebroventricular cannula, and both TIDA neuronal activity and serum prolactin level were determined. Nicotine (10 ng/3 microl/rat) given at 10:00 h significantly inhibited TIDA neuronal activity from 5 to 30 min and stimulated serum PRL levels at 5 and 15 min. Co-administration of either mecamylamine (1 microg) or naloxone (2.5 microg) prevented both nicotine's effects. A dose-related (0.1-100 ng) effect of nicotine on TIDA neuronal activity and serum PRL level was also observed in the morning when TIDA neuronal activity is high and serum PRL level is low, but not in the afternoon when the former activity is low and the latter is high. When atropine (20 microg), naloxone (25 microg) or Nor-BNI (20 microg) was given at 14:00 h all increased the lowered TIDA neuronal activity in the afternoon. When atropine was co-administered with either naloxone or Nor-BNI, however, no additive effect was observed. Submaximal doses of atropine (0.2 microg), mecamylamine (0.1 microg) or naloxone (0.25 microg) was also effective in stimulating the afternoon levels of TIDA neuronal activity and inhibiting serum PRL, and no additive effect was observed either. Moreover, simultaneous injection of morphine (15 microg) prevented atropine's effect in the afternoon. These results indicate that cholinergic neurons may act through activating the endogenous opioidergic neurons to exhibit an inhibitory effect on TIDA neuronal activity and a stimulatory one on prolactin secretion. A diurnal difference in its endogenous activity between morning and afternoon was also implicated.
Shieh
K R
KR
Department of Physiology, Schools of Life Science and Medicine, National Yang-Ming University, Taipei, Taiwan, ROC.
Pan
J T
JT
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism; D000818:Animals; D018678:Cholinergic Agents / Q000494:pharmacology; D002940:Circadian Rhythm; D004295:Dihydroxyphenylalanine / Q000378:metabolism; D004298:Dopamine / Q000502:physiology*; D004723:Endorphins / Q000502:physiology*; D005260:Female; D007031:Hypothalamus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D008473:Median Eminence / Q000378:metabolism; D009294:Narcotics / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D009538:Nicotine / Q000378:metabolism* / Q000494:pharmacology; D010052:Ovariectomy; D011388:Prolactin / Q000097:blood / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
D018678:Cholinergic Agents; D004723:Endorphins; D009294:Narcotics; D015102:3,4-Dihydroxyphenylacetic Acid; D004295:Dihydroxyphenylalanine; D009538:Nicotine; D011388:Prolactin; D004298:Dopamine