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Prolactin regulation of tuberoinfundibular dopaminergic neurons: immunoneutralization studies.
Brain Res. 2000 Jan 03; 852(1):28-36.BR

Abstract

The purpose of this study was to determine the effects of acute hypoprolactinemia on tuberoinfundibular dopamine (DA) neurons using a rabbit anti-rat prolactin antiserum (PRL-AB) to immunoneutralize circulating prolactin under basal conditions and at various times after haloperidol-induced hyperprolactinemia. The specificity of PRL-AB for prolactin was determined by examining the ability of unlabelled hormone to displace binding of 125I-labelled prolactin to PRL-AB. Tuberoinfundibular DA neuronal activity was estimated by measuring the concentrations of the DA metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence which contains terminals of these neurons. Systemic (i.v.) administration of 200 microl of PRL-AB decreased plasma prolactin concentrations below detectable levels for at least 4 h, and this was accompanied by a pronounced decrease in DOPAC concentrations in the median eminence of females, but not males. Central (i.c.v.) administration of 2 microl PRL-AB diluted up to 1:100 mimicked the inhibitory effect of systemic administration of PRL-AB on median eminence DOPAC concentrations suggesting that the tonic stimulatory effect of prolactin on the basal activity of tuberoinfundibular DA neurons in females occurs via a central site of action. In male rats, blockade of anterior pituitary DA receptors with haloperidol (1 mg/kg; s.c.) caused an prompt (by 1 h) increase in plasma prolactin concentrations which was maintained for at least 12 h. Haloperidol-induced hyperprolactinemia also caused a delayed (at 6 and 12 h) increase in median eminence DOPAC concentrations in these animals which was blocked by PRL-AB. Exposure of rats to initial priming periods of endogenous hyperprolactinemia of up to 6 h duration (followed by 6 h or more of PRL-AB-induced hypoprolactinemia) failed to alter median eminence DOPAC concentrations unless prolactin exposure was reinstated by an i.c.v. injection of prolactin. These results confirm that prolactin mediates the stimulatory effects of haloperidol on tuberoinfundibular DA neurons, and reveal that delayed induced activation of these neurons by prolactin is dependent upon a priming period of sustained hyperprolactinemia longer than 3 h for initiation and maintenance of this response.

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Authors+Show Affiliations

Hentschel K
Department of Pharmacology and Toxicology, Michigan State University, East Lansing 48824, USA.
Fleckenstein AE
No affiliation info available
Toney TW
No affiliation info available
Lawson DM
No affiliation info available
Moore KE
No affiliation info available
Lookingland KJ
No affiliation info available

MeSH

3,4-Dihydroxyphenylacetic AcidAnimalsArcuate Nucleus of HypothalamusDopamineDopamine AntagonistsFemaleHaloperidolHyperprolactinemiaImmune SeraInjections, IntravenousInjections, IntraventricularMaleMedian EminenceNeuronsPituitary Gland, AnteriorProlactinRatsRats, Long-EvansReceptors, Dopamine

Pub Type(s)

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

Language

eng

PubMed ID

10661492

Citation

Hentschel, K, et al. "Prolactin Regulation of Tuberoinfundibular Dopaminergic Neurons: Immunoneutralization Studies." Brain Research, vol. 852, no. 1, 2000, pp. 28-36.
Hentschel K, Fleckenstein AE, Toney TW, et al. Prolactin regulation of tuberoinfundibular dopaminergic neurons: immunoneutralization studies. Brain Res. 2000;852(1):28-36.
Hentschel, K., Fleckenstein, A. E., Toney, T. W., Lawson, D. M., Moore, K. E., & Lookingland, K. J. (2000). Prolactin regulation of tuberoinfundibular dopaminergic neurons: immunoneutralization studies. Brain Research, 852(1), 28-36.
Hentschel K, et al. Prolactin Regulation of Tuberoinfundibular Dopaminergic Neurons: Immunoneutralization Studies. Brain Res. 2000 Jan 3;852(1):28-36. PubMed PMID: 10661492.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Prolactin regulation of tuberoinfundibular dopaminergic neurons: immunoneutralization studies. AU - Hentschel,K, AU - Fleckenstein,A E, AU - Toney,T W, AU - Lawson,D M, AU - Moore,K E, AU - Lookingland,K J, PY - 2000/2/8/pubmed PY - 2000/2/26/medline PY - 2000/2/8/entrez SP - 28 EP - 36 JF - Brain research JO - Brain Res VL - 852 IS - 1 N2 - The purpose of this study was to determine the effects of acute hypoprolactinemia on tuberoinfundibular dopamine (DA) neurons using a rabbit anti-rat prolactin antiserum (PRL-AB) to immunoneutralize circulating prolactin under basal conditions and at various times after haloperidol-induced hyperprolactinemia. The specificity of PRL-AB for prolactin was determined by examining the ability of unlabelled hormone to displace binding of 125I-labelled prolactin to PRL-AB. Tuberoinfundibular DA neuronal activity was estimated by measuring the concentrations of the DA metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence which contains terminals of these neurons. Systemic (i.v.) administration of 200 microl of PRL-AB decreased plasma prolactin concentrations below detectable levels for at least 4 h, and this was accompanied by a pronounced decrease in DOPAC concentrations in the median eminence of females, but not males. Central (i.c.v.) administration of 2 microl PRL-AB diluted up to 1:100 mimicked the inhibitory effect of systemic administration of PRL-AB on median eminence DOPAC concentrations suggesting that the tonic stimulatory effect of prolactin on the basal activity of tuberoinfundibular DA neurons in females occurs via a central site of action. In male rats, blockade of anterior pituitary DA receptors with haloperidol (1 mg/kg; s.c.) caused an prompt (by 1 h) increase in plasma prolactin concentrations which was maintained for at least 12 h. Haloperidol-induced hyperprolactinemia also caused a delayed (at 6 and 12 h) increase in median eminence DOPAC concentrations in these animals which was blocked by PRL-AB. Exposure of rats to initial priming periods of endogenous hyperprolactinemia of up to 6 h duration (followed by 6 h or more of PRL-AB-induced hypoprolactinemia) failed to alter median eminence DOPAC concentrations unless prolactin exposure was reinstated by an i.c.v. injection of prolactin. These results confirm that prolactin mediates the stimulatory effects of haloperidol on tuberoinfundibular DA neurons, and reveal that delayed induced activation of these neurons by prolactin is dependent upon a priming period of sustained hyperprolactinemia longer than 3 h for initiation and maintenance of this response. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/10661492/Prolactin_regulation_of_tuberoinfundibular_dopaminergic_neurons:_immunoneutralization_studies_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(99)02182-4 DB - PRIME DP - Unbound Medicine ER -