Cortisol levels are positively associated with pup-feeding rates in male meerkats

In societies of cooperative vertebrates, individual differences in contributions to offspring care are commonly substantial. Recent attempts to explain the causes of this variation have focused on correlations between contributions to care and the protein hormone prolactin, or the steroid hormone testosterone. However, such studies have seldom considered the importance of other hormones or controlled for non-hormonal factors that are correlative with both individual hormone levels and contributions to care. Using multivariate statistics, we show that hormone levels explain significant variation in contributions to pup-feeding by male meerkats, even after controlling for non-hormonal effects. However, long-term contributions to pup provisioning were significantly and positively correlated with plasma levels of cortisol rather than prolactin, while plasma levels of testosterone were not related to individual patterns of pup-feeding. Furthermore, a playback experiment that used pup begging calls to increase the feeding rates of male helpers gave rise to parallel increases in plasma cortisol levels, whilst prolactin and testosterone levels remained unchanged. Our findings confirm that hormones can explain significant amounts of variation in contributions to offspring feeding, and that cortisol, not prolactin, is the hormone most strongly associated with pup-feeding in cooperative male meerkats

Cortisol levels are positively associated with pup-feeding rates in male meerkats

In societies of cooperative vertebrates, individual differences in contributions to offspring care are commonly substantial. Recent attempts to explain the causes of this variation have focused on correlations between contributions to care and the protein hormone prolactin, or the steroid hormone testosterone. However, such studies have seldom considered the importance of other hormones or controlled for non-hormonal factors that are correlative with both individual hormone levels and contributions to care. Using multivariate statistics, we show that hormone levels explain significant variation in contributions to pup-feeding by male meerkats, even after controlling for non-hormonal effects. However, long-term contributions to pup provisioning were significantly and positively correlated with plasma levels of cortisol rather than prolactin, while plasma levels of testosterone were not related to individual patterns of pup-feeding. Furthermore, a playback experiment that used pup begging calls to increase the feeding rates of male helpers gave rise to parallel increases in plasma cortisol levels, whilst prolactin and testosterone levels remained unchanged. Our findings confirm that hormones can explain significant amounts of variation in contributions to offspring feeding, and that cortisol, not prolactin, is the hormone most strongly associated with pup-feeding in cooperative male meerkats

The differential secretion of FSH and LH : regulation through genes, feedback and packaging

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Dopamine D1 receptor analogues act centrally to stimulate prolactin secretion in ewes

It is well known that prolactin secretion is inhibited by dopamine activity via the pituitary dopamine D2 receptor. Dopamine D1 receptor analogues also affect prolactin levels although the mechanisms and physiological significance are poorly understood. The present study of the ewe was undertaken to characterize the effects of the D1 receptor agonist SKF 38393 and antagonist SCH 23390 on prolactin in this species and to determine whether the prolactin response to both drugs requires an intact hypothalamo-pituitary axis. Ovariectomized ewes were injected intravenously with vehicle, 0.2, 2 or 20 mg SKF 38393 (D1 agonist) or SCH 23390 (D1 antagonist). At the 20 mg dose, plasma prolactin concentrations were significantly (P < 0.01) increased by each drug and returned within an hour to control levels. When injected directly into the lateral ventricles of the brain (intracerebroventricular (i.c.v.) injection), a 100-fold lower dose of SKF 38393 (0.2 mg; P < 0.05) was sufficient to stimulate prolactin secretion. In contrast, i.c.v. injection of SCH 23390 (0.02 and 0.2 mg) had no effect on prolactin levels and at no dose was there evidence for suppression of prolactin levels. These results are in accord with earlier studies in the rat which suggested that the D1 agonist stimulated prolactin secretion via a direct effect on central dopamine D1 receptors whereas the D1 antagonist interacted with the pituitary dopamine D2 receptor to increase prolactin secretion. In a further experiment this hypothesis was tested in hypothalamo-pituitary disconnected ewes which were infused with dopamine (0.5 microgram/kg per min) for 3 h.(ABSTRACT TRUNCATED AT 250 WORDS