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Time-dependent increase in plasma prolactin after pituitary stalk section: role of posterior pituitary dopamine.
Endocrinology. 1989 May; 124(5):2343-9.E

Abstract

PRL secretion is inhibited by dopamine (DA) input from two systems: the tuberoinfundibular (TIDA) with terminals in the median eminence, and the tuberohypophyseal (THDA) with terminals in the posterior pituitary. The aims of this study were 1) to determine the effects of pituitary stalk section (SS), which prevents DA input from the TIDA neurons, on PRL release, and 2) to assess if the anterior pituitary receives any DA input after SS. Ovariectomized rats were subjected to SS or sham surgery. Jugular blood was collected on the day of surgery (day 0) and for 6 days thereafter and was analyzed for PRL by RIA. DA concentration in the posterior pituitary was determined by HPLC. Unexpectedly, SS caused only a 2- to 3-fold initial rise in plasma PRL on day 0. This was followed by a gradual rise to 4-, 6-, and 8-fold above control levels on days 2, 4, and 6, respectively, without a further increase by 2 weeks. During this time, DA concentrations in the posterior pituitary progressively declined to 66%, 28%, and 6% of control values on days 1, 2, and 6 after SS, respectively. In the second experiment, intact and SS rats were treated with the DA receptor antagonist haloperidol. Haloperidol induced a dramatic 30- to 40-fold increase in plasma PRL in intact rats. Haloperidol induced a 3-fold rise in plasma PRL on day 1 after SS and a transient 2.5-fold rise on day 2. On day 6 after SS, when DA in the posterior pituitary was barely detectable, haloperidol failed to increase PRL secretion. The DA agonist apomorphine caused similar inhibitions of PRL release on days 1 and 6 after SS. Injections of TRH stimulated PRL secretion equally well in intact and SS rats. We conclude that SS does not induce refractoriness to PRL secretagogues or a dysfunction of the anterior pituitary DA receptors. The immediate rise in PRL after SS is modest because the anterior pituitary still receives DA input from the posterior pituitary. A gradual exhaustion of posterior pituitary DA, caused by the disconnection of the THDA terminals from their perikarya, leads to the progressive rise in plasma PRL levels. The DA input affecting PRL release is derived exclusively from the TIDA and THDA neurons, but their relative contributions are yet unknown.

Authors+Show Affiliations

Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis 46223.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

2495929

Citation

Murai, I, et al. "Time-dependent Increase in Plasma Prolactin After Pituitary Stalk Section: Role of Posterior Pituitary Dopamine." Endocrinology, vol. 124, no. 5, 1989, pp. 2343-9.
Murai I, Garris PA, Ben-Jonathan N. Time-dependent increase in plasma prolactin after pituitary stalk section: role of posterior pituitary dopamine. Endocrinology. 1989;124(5):2343-9.
Murai, I., Garris, P. A., & Ben-Jonathan, N. (1989). Time-dependent increase in plasma prolactin after pituitary stalk section: role of posterior pituitary dopamine. Endocrinology, 124(5), 2343-9.
Murai I, Garris PA, Ben-Jonathan N. Time-dependent Increase in Plasma Prolactin After Pituitary Stalk Section: Role of Posterior Pituitary Dopamine. Endocrinology. 1989;124(5):2343-9. PubMed PMID: 2495929.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Time-dependent increase in plasma prolactin after pituitary stalk section: role of posterior pituitary dopamine. AU - Murai,I, AU - Garris,P A, AU - Ben-Jonathan,N, PY - 1989/5/1/pubmed PY - 1989/5/1/medline PY - 1989/5/1/entrez SP - 2343 EP - 9 JF - Endocrinology JO - Endocrinology VL - 124 IS - 5 N2 - PRL secretion is inhibited by dopamine (DA) input from two systems: the tuberoinfundibular (TIDA) with terminals in the median eminence, and the tuberohypophyseal (THDA) with terminals in the posterior pituitary. The aims of this study were 1) to determine the effects of pituitary stalk section (SS), which prevents DA input from the TIDA neurons, on PRL release, and 2) to assess if the anterior pituitary receives any DA input after SS. Ovariectomized rats were subjected to SS or sham surgery. Jugular blood was collected on the day of surgery (day 0) and for 6 days thereafter and was analyzed for PRL by RIA. DA concentration in the posterior pituitary was determined by HPLC. Unexpectedly, SS caused only a 2- to 3-fold initial rise in plasma PRL on day 0. This was followed by a gradual rise to 4-, 6-, and 8-fold above control levels on days 2, 4, and 6, respectively, without a further increase by 2 weeks. During this time, DA concentrations in the posterior pituitary progressively declined to 66%, 28%, and 6% of control values on days 1, 2, and 6 after SS, respectively. In the second experiment, intact and SS rats were treated with the DA receptor antagonist haloperidol. Haloperidol induced a dramatic 30- to 40-fold increase in plasma PRL in intact rats. Haloperidol induced a 3-fold rise in plasma PRL on day 1 after SS and a transient 2.5-fold rise on day 2. On day 6 after SS, when DA in the posterior pituitary was barely detectable, haloperidol failed to increase PRL secretion. The DA agonist apomorphine caused similar inhibitions of PRL release on days 1 and 6 after SS. Injections of TRH stimulated PRL secretion equally well in intact and SS rats. We conclude that SS does not induce refractoriness to PRL secretagogues or a dysfunction of the anterior pituitary DA receptors. The immediate rise in PRL after SS is modest because the anterior pituitary still receives DA input from the posterior pituitary. A gradual exhaustion of posterior pituitary DA, caused by the disconnection of the THDA terminals from their perikarya, leads to the progressive rise in plasma PRL levels. The DA input affecting PRL release is derived exclusively from the TIDA and THDA neurons, but their relative contributions are yet unknown. SN - 0013-7227 UR - https://www.unboundmedicine.com/medline/citation/2495929/Time_dependent_increase_in_plasma_prolactin_after_pituitary_stalk_section:_role_of_posterior_pituitary_dopamine_ L2 - https://academic.oup.com/endo/article-lookup/doi/10.1210/endo-124-5-2343 DB - PRIME DP - Unbound Medicine ER -