Opiate Modulation of the Anterior Pituitary Hormone Response during Suckling in the Rat*
Peter Riskind, William J. Millard, Joseph B. Martin
Abstract
Peter Riskind, William J. Millard, Joseph B. Martin
Abstract
We have investigated the influence of endogenous opiates on hormone responses during suckling in the rat. In complementary experiments, opiate receptors were blocked by naloxone (NAL) or endogenous opiate release from the pituitary was inhibited by dexamethasone (DEX). Serial blood samples from unanesthetized suckled rats were then assayed for plasma PRL, beta-endorphin-like immunoreactivity (beta-END-LI), TSH, and GH levels. Identical studies were also done in saline-treated (control) suckled rats and in unsuckled rats exposed to control objects. Whereas suckling caused a rise in plasma PRL, beta-END-LI, and GH, introduction of plastic control objects did not elevate hormone levels. NAL blocked the GH rise and depressed TSH levels, but did not significantly inhibit the PRL or beta-END-LI response. DEX prevented the beta-END-LI rise and blocked the GH rise, but did not inhibit TSH. DEX enhanced PRL release during suckling. These results demonstrate that 1) the responses of beta-END-LI, PRL, and GH are not an artifact of the sampling procedure; 2) PRL release during suckling is independent of beta-END-LI release by the pituitary; and 3) suckling stimulates the release of ACTH, beta-END, and beta-lipotropin from the anterior pituitary. Our results are consistent with both a role of pituitary beta-END in the control of GH and a role of corticosterone in the control of PRL during suckling.
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We have investigated the influence of endogenous opiates on hormone responses during suckling in the rat. In complementary experiments, opiate receptors were blocked by naloxone (NAL) or endogenous opiate release from the pituitary was inhibited by dexamethasone (DEX). Serial blood samples from unanesthetized suckled rats were then assayed for plasma PRL, beta-endorphin-like immunoreactivity (beta-END-LI), TSH, and GH levels. Identical studies were also done in saline-treated (control) suckled rats and in unsuckled rats exposed to control objects. Whereas suckling caused a rise in plasma PRL, beta-END-LI, and GH, introduction of plastic control objects did not elevate hormone levels. NAL blocked the GH rise and depressed TSH levels, but did not significantly inhibit the PRL or beta-END-LI response. DEX prevented the beta-END-LI rise and blocked the GH rise, but did not inhibit TSH. DEX enhanced PRL release during suckling. These results demonstrate that 1) the responses of beta-END-LI, PRL, and GH are not an artifact of the sampling procedure; 2) PRL release during suckling is independent of beta-END-LI release by the pituitary; and 3) suckling stimulates the release of ACTH, beta-END, and beta-lipotropin from the anterior pituitary. Our results are consistent with both a role of pituitary beta-END in the control of GH and a role of corticosterone in the control of PRL during suckling.
Key concepts: Internal medicine, Endocrinology, Anterior pituitary, Opiate, Endogeny, (+)-Naloxone, Prolactin, Endogenous opioid