Modification of behavioral estrus in the guinea pig following intracranial cycloheximide

Wallen, Kurt; Goldfoot, David A.; Joslyn, W D; Paris, Charles A.

doi:10.1016/0031-9384(72)90364-2

Cited by 29 publications

(3 citation statements)

References 7 publications

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“…If there were no correlation between the amount of receptor translocated to nuclei and the level of sexual behavior, it would be difficult to argue that P acted through genomic mechanisms to acti vate proceptive behavior. But as it stands, the data comple ment the observations that inhibitors of RNA or protein synthesis will block the activation of sexual behavior or LH secretion by P [11,26,29,35], and thus strengthen the no tion that the neural effects of P might be mediated by gene activation. The identification of gene products in the MBH-POA that are influenced by P, and the determination of their role in neuronal function would provide additional evidence that the behavioral effects of P are mediated through nuclear translocation.…”

Section: Discussionsupporting

confidence: 56%

“…This hypothesis is supported by observatio. -that inhibitors of RNA and protein synthesis can block tl • actions of Pon lordosis behavior and LH release [11,26,29,35]. However, there are only a few studies which demo: -strate or imply that nuclear translocation of progestin rceptors can occur in brain tissue [3,4, 14], and there is amost no information about the causal relationship of this process to the neural effects of P. In this study, we have ust 1 an in vitro exchange assay to evaluate under different coditions the movement of cytoplasmic progestin recepto s into the nuclear fraction of brain tissue.…”

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confidence: 99%

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Nuclear Progestin Receptors in Rat Brain and Pituitary

et al. 1982

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Progestin receptors in rat brain and pituitary cell nuclei were measured with an in vitro exchange assay in order to examine the role of estrogen priming and of endogenous and exogenous progesterone in determining the amount of receptor which reaches the nuclear compartment. Progesterone administration causes progestin receptors, demonstrable by exchange, to appear in the cell nuclear fraction from rat pituitary, hypothalamus-preoptic area (HYP-POA), and cerebral cortex, all of which contain cytosol progestin receptor sites. The amount of progestin receptor translocated to nuclei by 1 mg of progesterone increases after estrogen priming in pituitary and HYP-POA, tissues which contain progestin receptors inducible by estradiol. The increase in nuclear progestin receptors after progesterone is proportionally the same in estrogen-primed and in unprimed HYP-POA as well as in the cerebral cortex, where noninducible progestin receptors are found. Further characterization of nuclear progestin receptors reveals that those translocated to cell nuclei are differentialy extracted by 0.4 M KCl and that high estrogen treatment in the absence of progesterone appears to give rise to some progestin receptor translocation to nuclei. The influence of both estrogen priming and progesterone release is evident in HYP-POA and pituitary cell nuclei assay by progestin exchange from rats killed at various stages of the estrous cycle. The amount of nuclear progestin receptor increases from diestrus to noon on proestrus, due apparently to endogenous estrogen priming, since progesterone levels remain the same and cytosol progestin receptors are known to increase in this time. Nuclear progestin receptors increase from noon to 16:30 h on proestrus in parallel with the proestrus rise of progesterone. This increase precedes the normal appearance of estrous behavior on the evening of proestrus. When estrogen-primed ovariectomized rats are given varying doses of progesterone and tested for sexual behavior or killed for progestin receptor exchange assays, nuclear progestin receptors are found to increase in the same way as the dose dependence of proceptive sexual behavior. Thus, the translocation of progestin receptors to MBH-POA cell nuclei may be an important step in the activation of proceptive sexual behavior by progesterone.

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Section: Discussionsupporting

confidence: 56%

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confidence: 99%

Nuclear Progestin Receptors in Rat Brain and Pituitary

et al. 1982

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“…1, No. 5, May 1981 Antibiotics have been employed successfully as reversible inhibitors of steroid-induced changes in sexual receptivity and proceptivity (Wallen et al, 1972;Quadagno and Ho, 1975;Rainbow et al, 1980;Parsons et al, 1981b). We have presented evidence elsewhere that a discontinuous estradiol treatment, in two 1-hr segments, is sufficient to activate the lordosis reflex 24 hr after the initiation of estradiol treatment (Parsons et al, 1981b).…”

Section: Resultsmentioning

confidence: 99%

Sequential inhibition of sexual receptivity by progesterone is prevented by a protein synthesis inhibitor and is not causally related to decreased levels of hypothalamic progestin receptors in the female rat

Parsons¹,

McEwen²

1981

J. Neurosci.

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In the estrogen-primed ovariectomized female rat, the administration of progesterone facilitates sexual receptivity and activates proceptivity for many hours. If the progesterone dose is large (e.g., 2.5 mg), a refractory period follows, during which time animals are less sensitive to additional progesterone. This refractory period has been termed "sequential inhibition" and has been correlated previously with decreased levels of cytosol progestin receptors in the mediobasal hypothalamus-preoptic area (MBH-POA). Our present results indicate that the "sequential inhibition" of mating behavior by progesterone appears to involve a protein synthetic step that is not related causally to decreased levels of cytosol progestin receptors in the MBH-POA. Animals which received subcutaneous injections of the protein synthesis inhibitor, anisomycin (100 mg/kg in saline), 15 min prior to and again 3 hr after progesterone (2.5 mg in propylene glycol) treatment, displayed greater sexual receptivity at 24 hr than did animals which received subcutaneous saline injections. However, cytosol progestin receptor levels in the MBH-POA of animals which received anisomycin plus progesterone were decreased at 24 hr, relative to animals which received saline plus progesterone. Anisomycin did not produce positive or negative behavioral effects at 24 hr when administered 15 min prior to and again 3 hr after propylene glycol, suggesting that the behavioral effects of anisomycin appear to be related to selective blockade of progesterone action. In separate experiments, we administered single subcutaneous injections of anisomycin at various times relative to progesterone (2.5 mg) treatment. According to the time course of effective anisomycin application, the presumed protein synthesis which is responsible for the inhibition of mating behavior occurs between 3 and 13 hr after the administration of progesterone.

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Some Aspects of the Neuroendocrine Regulation of Mammalian Sexual Behaviour

Larsson¹,

Beyer²

1981

Neuroendocrine Regulation and Altered Behaviour

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Modification of behavioral estrus in the guinea pig following intracranial cycloheximide

Cited by 29 publications

References 7 publications

Nuclear Progestin Receptors in Rat Brain and Pituitary

Nuclear Progestin Receptors in Rat Brain and Pituitary

Sequential inhibition of sexual receptivity by progesterone is prevented by a protein synthesis inhibitor and is not causally related to decreased levels of hypothalamic progestin receptors in the female rat

Some Aspects of the Neuroendocrine Regulation of Mammalian Sexual Behaviour

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