The Neurologic Basis for the Anovulation of the Luteal Phase, Lactation and Pregnancy

Rothchild, I.

doi:10.1007/978-1-4899-6377-2_2

Cited by 12 publications

(6 citation statements)

References 46 publications

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“…Although increased prolactin and suppressed gonadotropin secretions characterize lactation there is little evidence to suggest that prolac tin is the suppressive factor. Rothchild (1960;1967) proposed that suck ling depresses the synthesis of gonadotropins while progesterone primarily inhibits their release, and suggested that the mechanism through which the suckling stimulus acts to prevent ovulation is neural and acts via centers in the hypothalamus. Ovulation cycles eventually reappear if milk secretion is prolonged by providing a succession of younger foster pups, regardless of the mechanism of suppressed ovarian activity during lacta tion (Bruce, 1961).…”

Section: Literature Reviewmentioning

confidence: 99%

Gonadotropin Levels in Lactating Rats: Effect of Ovariectomy12

Ford

Melampy

1973

Endocrinology

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Section: Literature Reviewmentioning

confidence: 99%

Gonadotropin Levels in Lactating Rats: Effect of Ovariectomy12

Ford

Melampy

1973

Endocrinology

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“…Because the act of incubation seems to stimulate prolactin secretion (Eisner, 1960;Jones, 1969 b) it would be enlightening to investigate the possibility that tactile stimulation of the sensitized skin of the incubation patch causes prolactin release. One is immediately reminded of the release of prolactin by stimulation of the oestrogensensitized nipple in mammals (Rothchild, 1966). The dermis and the basal layer of the epidermis of birds are richly supplied with sensory receptors either existing as dense networks of nerve endings or as specialized sensory corpuscles (Schartau, 1938;Portman, 1961 ;Winklemann & Myers, 1961).…”

Section: (3) Patch Formation and Behaviourmentioning

confidence: 99%

The Incubation Patch of Birds

Jones¹

1971

Biological Reviews

129

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Summary 1. The incubation patch of birds forms in the areas of the ventrum devoid of contour feathers (apteria) by processes involving defeathering of down, dermal and subdermal hypervascularization, oedema, and hyperplasia of the epidermis and dermal connective tissue. Its formation facilitates the transfer of heat to the eggs and hatched young. 2. In general, the sex that incubates develops a patch; this may be the female, both sexes, or the male, and the species within any one order tend to exhibit a common pattern. In some orders (e.g. Pelecaniformes) no patch develops. 3. The incubation patch begins to form before egg laying in passerine birds and during egg laying in Galliformes. Most of the patch responses in passerines are completed earlier in the reproductive cycle (late egg laying to middle incubation) than in Galliformes (middle incubation to early brooding). 4. In the passerines studied, in which usually only the female develops a patch, oestrogen and prolactin synergize to cause patch development; oestrogen given alone is effective because it synergizes with endogenous prolactin in intact birds. The role of progesterone is unclear, but it seems to mimic the effects of prolactin and also plays a role in the increase in skin sensitivity characteristic of patch development in the canary. 5. In the one galliform studied (California quail), in which both sexes develop a patch, either oestrogen or androgen synergizes with prolactin; oestrogen alone is ineffective in non‐breeding quail because of insufficient endogenous prolactin levels. Prolactin alone causes epidermal hyperplasia and vascularization, and progesterone seems mainly to be involved in defeathering. In the starling also both sexes develop a patch, but testosterone plus prolactin is not effective as it is in the quail. 6. In the phalaropes, birds in which only the male develops a patch, androgen and prolactin are the effective synergists in patch development. Thus, there is a correlation between the sex which develops a patch in the wild and the steroid (oestrogen or androgen) which synergizes with prolactin. 7. In the brown‐headed cowbird, a parasitic species which neither develops a patch nor incubates, there are no responses to exogenous hormones. The absence of patch development in one sex or in both can be due either to an absence of appropriate hormone levels or to a lack of sensitivity of the skin to hormones. 8. More study is needed of the transfer of heat from the patch area to the eggs or young, including the relationships between patch structure, surface area, surface temperature, type of nest, and the number and size of eggs. 9. Patch formation is affected by and influences behaviour. 10. More research is needed in regard to (I) the natural development and endocrine control of the incubation patch in various orders of birds: (2) the effects of patch formation on behaviour, and vice versa; (3) the mode of action of the hormones in patch formation, that is, whether it is direct or indirect, e.g. through the release of another hormone;...

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“…Both progesterone and ICI 33828 appear to block the lh surge late in the oestrous cycle (Garbers & First, 1969a), and both probably have a major influence on the hypothalamus. The effects on appetite, however, are opposite (Harrington & Linkenheimer, 1966;Rothchild, 1967). A tendency for ICI 33828 treatment to cause lower pituitary prolactin levels than pro¬ gesterone treatment at Day 14 of the oestrous cycle in gilts has been reported, and may also indicate differential effects of the two compounds on prolactin release (Garbers & First, 1969a).…”

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confidence: 90%

“…Therefore, antagonism of prolactin secretion by high levels of progesterone in the presence of exogenous oestrogen might account for the reduction in cl size and weight by progesterone. Progesterone, however, is thought to act in a positive feedback with prolactin (Rothchild, 1967). Both progesterone and ICI 33828 appear to block the lh surge late in the oestrous cycle (Garbers & First, 1969a), and both probably have a major influence on the hypothalamus.…”

mentioning

confidence: 97%

“…The pituitary is required, since oestrogen will not maintain cl in the gilt in which the pituitary stalk has been transected (Anderson, Dyck, Mori, Henricks & Melampy, 1967). Oestrogen blocks pituitary lh and fsh release, and Rothchild (1966) has therefore suggested that increased prolactin release due to oestrogen may maintain the corpora lutea in the intact gilt. Prolactin, however, will not delay cl regression in the hypophysectomized pig (Du Buisson, Leglise, Anderson & Rombauts, 1964).…”

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