Immunoreactive Prolactin in the Hypothalamus and Cerebrospinal Fluid of Male and Female Rats

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Abstract
Immunoreactive prolactin (ir-PRL) has been identified in the cerebrospinal fluid (CSF) and brain of the male and female rats. In this study we determined the concentration of ir-PRL in the CSF and hypothalamus under conditions known to increase or decrease serum PRL. Hypophysectomy (60 days) significantly decreased the concentration of ir-PRL in the CSF of male (4.9 .+-. 0.7 vs. 3.0 .+-. 0.3 ng/ml) female (5.8 .+-. 0.9 vs. 3.1 .+-. 0.5 ng/ml) rats. However, the effect of long-term hypophysectomy on hypothalamic ir-PRL was gender-dependent. That is, in the male rat hypophysectomy did not affect the content of ir-PRL in the median eminence, ventral hypothalamus. In contrast, in the female rat, long-term hypophysectomy decreased the content of ir-PRL in the median eminence, ventral hypothalamus, and dorsal hypothalamus 37, 40, and 47%, respectively. Estradiol replacement to the hypophysectomized female rat normalized the content of ir-PRL in the median eminence (96 .+-. 5.8 to 131 .+-. 9.6 ng/mg protein), ventral hypothalamus (11 .+-. 0.6 to 16.0 .+-. 1.1 ng/mg protein), dorsal hypothalamus (4.7 .+-. 0.04 to 8.6 .+-. 0.4 ng/mg protein), and the concentration ir-PRL in the CSF (2.5 .+-. 0.3 to 4.6 .+-. 0.4 ng/ml). In intact female rats, administration of haloperidol induced a marked hyperprolactinemia, and significantly increased CSF ir-PRL (5.1 .+-. 1.5 vs. 18.0 .+-. 3.8 ng/ml). However, in the same rats, the content of ir-PRL in the median eminence was significantly decreased while the ir-PRL content in the ventral hypothalamus and dorsal hypothalamus was unaffected. Administration of haloperidol to hypophysectomized females rats did not affect the concentration of ir-PRL in the CSF, but decreased the contentof ir-PRL in the median eminence (83.0 .+-. 7.3 to 62.6 .+-. 6.8 ng/mg protein). The detection of ir-PRL in the CSF of hypophysectomized male and female rats indicates that CSF ir-PRL is not completely dependent on plasma ir-PRL. The increase in CSF and hypothalamic ir-PRL in estradiol-, but not haloperiodol-, treated hypophysectomized female rats indicates that hypothalamic and CSF ir-PRL is regulated by an estrogen-dependent mechanism at an extrapituitary site. In addition, the failure of hypothalamic ir-PRL to parallel changes in either plasma or CSF ir-PRL indicates that hypothalamic ir-PRL is not derived from the plasma or CSF. In contrast, this study suggests that hypothalamic ir-PRL may be one source of CSF PRL.