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The Anterior Pituitary-Grafted Rat: A Valid Model of Chronic Hyperprolactinemia^*

Endocrinology and Metabolism Section, McGuire Veterans Administration Medical Center and Department of Medicine, Medical College of Virginia Richmond, Virginia 23249

Correspondence: Address requests for reprints and all correspondence to: Dr. Robert A. Adler, Chief, Endocrinology and Metabolism (111-P), McGuire Veterans Administration Medical Center, Richmond, Virginia 23249.

Abstract

TRANSPLANTATION of the rat anterior pituitary gland to the kidney capsule results in a state of chronic hyperprolactinemia. For more than 35 yr two versions of this model have been used to study the functions of PRL. Autotransplantation of the pituitary to the kidney capsule induces hyperprolactinemia, but growth, GH secretion, and other anterior pituitary functions are diminished. Nonhypophysectomized rats implanted with anterior pituitary glands from littermate donors also have excess circulating PRL levels, but growth, GH secretion, and thyroid function remain normal. In the intact pituitary-grafted male rat, gonadal testosterone secretion is maintained despite diminished gonadotropin secretion. One shortcoming of the intact pituitary-grafted rat is glucocorticoid excess, the mechanism of which is unclear. However, adrenalectomy with adrenal steroid replacement of pituitary-grafted rats provides an animal model that appears to have one abnormality only, excess PRL secretion. This animal preparation compares favorably with other models used to study the many actions of PRL.

Footnotes

^* Studies with this model have been supported by NIH Grants R01- AM-22032, K01-AM-00707, S07-RR-05392, by a Merit Review Grant from the Veterans Administration, by the A. D. Williams Fund of the Medical College of Virginia, and by a grant from Innovative Research of America.

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