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  • Title: Stimulatory effect of central oxytocin on tuberoinfundibular dopaminergic neuron activity and inhibition on prolactin secretion: neurochemical and electrophysiological studies.
    Author: Yuan ZF, Pan JT.
    Journal: Endocrinology; 1996 Oct; 137(10):4120-5. PubMed ID: 8828466.
    Abstract:
    The posterior pituitary hormone, oxytocin (OT), has been shown to have either a stimulatory or an inhibitory effect on PRL secretion depending on the route of administration. Whether its central inhibitory effect involves the tuberoinfundibular dopaminergic (TIDA) neuron was the focus of this study. Adult female Sprague-Dawley rats ovariectomized for 1 week, implanted with sc estrogen-containing capsules and intracerebroventricular cannulas for 6 more days were used. TIDA neuron activity was determined by measuring the concentration of 3,4-dihydroxyphenylacetic acid or 3,4-dihydroxyphenylalanine in the median eminence by HPLC with electrochemical detection. Intracerebroventricular injection of OT induced both dose (0.01-1 microgram/rat)- and time (30-90 min)-dependent increases in 3,4-dihydroxyphenylalanine or 3,4-dihydroxyphenylacetic acid levels in the median eminence. Serum PRL levels were also decreased 30 min after the injection. The use of a specific OT antagonist, [d(CH2)5, Tyr(Me)2, Orn8]vasotocin, not only blocked the effect of OT on TIDA neuron activity, it further lowered it to below control levels, indicating the existence of an endogenous OT activity. When 1 microgram OT was administered at 1200 h, it also reversed the diurnal decrease in TIDA neuron activity at 1500 h. The effects of OT on the electrical activities of dorsomedial arcuate neurons were also tested using single unit recording in brain slices. In 33 neurons tested with OT, 66.7% were stimulated by OT in 0.5- to 50-nmol doses, and no inhibitory effect was observed. The rest were not responsive. In conclusion, both neurochemical and electrophysiological studies demonstrated that central OT may play a stimulatory role in regulating the TIDA neurons and, in turn, inhibition of PRL secretion.
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